Exam 1&2 study guide; Final exam notes and images
Exam 1&2 study guide; Final exam notes and images NSCI
Popular in Brain and Behavior
Popular in Department
verified elite notetaker
verified elite notetaker
verified elite notetaker
Educational Foundations 230
verified elite notetaker
verified elite notetaker
verified elite notetaker
This 109 page Study Guide was uploaded by Kimberley Notetaker on Wednesday September 16, 2015. The Study Guide belongs to NSCI at Tulane University taught by Dr. Jill M. Daniel in Fall 2015. Since its upload, it has received 177 views.
Reviews for Exam 1&2 study guide; Final exam notes and images
These are great! I definitely recommend anyone to follow this notetaker
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 09/16/15
Brain and Behavior 03242015 I Introduction 0 Relationship between brain and behavior 0 Differences between malefemale hormonesbrain structure 0 Psychology study of behavior and mental processes 0 Neurosciencel study of the nervous system Neurobiology genetics neuropharmacology neuroanatomy etc II The MindBrain Problem Are they the same Philosophical Issues 0 Dualism different separate and distinct o Monism same Psychoneural Identity Hypothesis 0 Modern take on monism o Psychological processes can be explained in terms of the underlying neural events 0 View of most neuroscientists III Levels of Analyses Molecular and cellular of neurons Neuron Integration 0 Systems How areas of the brain interact with each other IV Approaches Human Studies 0 Animal Studies 0 Use of model systems species that are studied to understand the biology of another organism l Neural Conduction Information that s travelling within a neuron Usually Dendrites l Terminal buttons End of axon Through electricity 0 1791 Luigi Gelpani 0 When lightning struck the wire frog legs twitched o 1874 Cincinnati physician woman with skull de cit electrically stimulated her brain l involuntary movement ll Electricity 0 De nition 0 A ow of electrons from a body that contains more electrons to a body that contains fewer electrons 0 Measured in volts 0 Nervous system millivolts Negative Pole 0 The body with the higher number of electrons o Negatively charged Positive Pole 0 The body with fewer electrons o Positively charged Electrical Potential 0 The difference in charge between the negative and positive poles 0 Measured in volts millivolts in nervous system 0 Potential for negative electrons to travel to the positive side lll Movement of ions create electrical charges 0 Ion 0 Simply a charged particles 0 Positively or negatively charged 0 Concentration Gradient 0 Passive charges 0 Flow naturally 0 Difference in distribution of various ions inside of the cell and outside the cell a particular ion will ow from an area of high concentration to an area of low concentration 0 Voltage or Electrical Gradient 0 When there s a difference of distribution of charges of ions from the inside of the cell and the outside of the cell they ll move from an area of high charge to an area of low charge 0 Positive ions want to go the negative side and vice versa 0 Force of voltage gradient would result in ow of negative ions from area of high charge to area of low charge Equilibrium 0 Force of the concentration gradient is equal to the force of the electrical gradient in opposing directions 0 No ow of ions 0 Only ow if the channel is open 0 When the force of the concentration force of voltage gradient movement of ions stop equilibrium IV Methods for recording activity of a neuron Neuroelectrophysiologists Membrane potential 0 The difference in charge between the inside of the cell and the outside of the cell V Resting potential of a neuron Difference in electrical charge across the membrane of an undisturbed neuron Difference in charge is 70 millivolts Resting potential is 70 millivolts Inside of the cell is 70 relative to the outside negative pole Selective Permeability O O O O 0 Some particles can go through and others cannot Without it you d reach equilibrium with a charge of zero and no membrane potential no electricity no functioning brain Maintains resting potential Determines what channels are open Some things can freely ow and some things can t Voltage gated Channels 0 O O O 0 Speci c ion channels for speci c ions Embedded in the membrane and allow ion to ow through if they re open Opened or closed depending upon the membrane potential Proteins embedded in the membrane which allow ions to ow in or out Respond to the charge by having a conformational change Relative Concentrations of Intracellular and Extracellular lons O O 0 If the inside of the cell is 70 it s going to pull in positive Na Sodium positive ion Cl Chloride negative K Potassium positive Negatively charged proteins No channels for these stuck inside the cell Passive Forces 0 Natural ow driven by the concentration gradient and the electrical gradient 0 Negatively charged particles make the inside of the cell negatively charged 0 Don t require energy 0 Active forces Sodiumpotassium pump 0 Protein embedded in the membrane 0 Maintain the 70 charge at resting potential 0 Working at all times to take 3 sodiums out and put 2 potassiums back in to maintain the balance 0 Status of Ion Channels 0 At resting potential sodium channels are closed 0 Potassium channels are mostly not entirely closed 0 Chloride channels are open but don t affect much because chloride is at equilibrium VI Graded Potentials De nition 0 Slight changes in the voltage across the neuron s membrane Hyperpolarization 0 Causes increased negativity bigger change 71 Depolarization o Decrease in difference between inside and outside of cell 0 Eg 70 l 69 slightly more positive VII Action Potential 0 De nition 0 A large brief reversing charge in the voltage of a neuron 0 Brie y the inside of the cell is positive relative to the outside of the cell 0 Threshold Potential o The voltage level at which an action potential is triggered About 65 Axon Hillock O 0 An area where the axon exits the cell body Adjacent to where the action potential is triggered l axon initial segment Status of Ion Channels 0 O O 0 When the charge across the membrane is 65 sodium channels open rapidly at threshold potential sodium rushes in Potassium channels start to open slowly During action potential the charge at the inside of the cell brie y goes up to about 50 The ow of sodium ions into the cell drives the action potential Flow of Ions Allornone Law 0 The action potential is dependent upon the opening of voltage gated sodium channels 0 The size or intensity of an action potential is independent of O the stimulus that created it If you reach 65 you ll have an action potential if you have a stronger charge it won t be a stronger action potential peak is about 50 VIII Repolarization Repolarization O O 0 When AP reaches its peak you get repolarization 50 Sodium channels close open at 65 close at 50 Potassium channels fully open ows out Flow of Ions 0 Potassium ows out close at 70 Hyperpolarization 0 Potassium channels start to close and you get a brief hyperpolarization IX Refractory Period 0 De nition 0 Phase following action potential during which the cell resists production of more action potential 0 Absolute 0 Sodium channels are closed rst part of the Refractory Period 0 Will not open no matter what stimulation is provided 0 Relative 0 Second part of the Refractory Period 0 Higher than normal level of stimulation is required to open the sodium channels and initiate a new action potential X Propagation of Action Potential 0 Description 0 Once an action potential occurs at one end of the axon axon hillock it depolarizes the part of the axon adjacent to it triggering those sodium channels to open 0 Initial segment repoarizes o Flows down the axon chain reactionwave o Maintains its strength all the way down the axon Implications of the Refractory Period 0 The Refractory Period results in two important characteristics of neural activity AP is normally unidirectional Rate of AP is related to intensity of stimulation Determinants of speed at which action potential travels 0 Diameter of axon The bigger the diameter the faster the speed More surface area more sodium channels Thinnest axon l 1 msec thickest l 10 msec 0 Presence of myelin sheath Fatty tissue that insulates many axons Faster conductions if an axon has myelin sheath n Nodes of Ranvier n Saltatory Conduction An action potential at the node triggers ow of current to the next node where the membrane regenerates the action potential XI Excitatory and inhibitory postsynaptic potentials EPSPs amp IPSPS De nition 0 O O O 0 Brief depolarizing or hyperpolarizing graded potentials Depolarizing input makes it more likely to get towards 65 threshold potential l excitatory Hyperpolarizing input makes the difference bigger more negative l inhibitory Only affecting a small area a few sodium channels open eg 70 l 69 Chloride channels may open chloride enters and gets the cell back to 70 In response to EPSPS Spatial Summation 0 000 0 Repeated stimui produced simultaneously at different synapses will add together sodium channels will open Figure 43 Two simultaneous EPSPs sum to produce a greater EPSP Two simultaneous lPSPs sum to produce a greater IPSP A simultaneous IPSP and EPSP cancel each other out 0 Temporal Summation O O O Stimuli produced in rapid succession at the same synapse will add together Figure 44 Two EPSPs elicited in rapid succession sum to produce a larger EPSP Two lPSPs elicited in rapid succession sum to produce a larger IPSP Relationship to Action Potential 0 The likelihood of an action potential occurring results in the sum of all of these o If it reaches 65 summation you get an action potential I A little history Debate whether the communication between neurons is electrical or chemical Sparkers vs Soupers o Sparkers electrical charge jumped across the synapse Soupers chemical signal traveled across the synapse 1920 sLoewi and Daleevidence for chemical transmission in peripheral nervous system heart study What about central nervous system 1940 sBoth sides agree that AP in one cell results in graded potential in next cell but how 1950 sSoupers win electrical signal l chemical l electrical Terms Presynaptic and Postsynaptic Neurons o Presynaptic neuron that sends the information o Postsynaptic neuron that s receiving the signal 0 Typically postsynaptic membrane is a dendritecell body 0 Presynaptic axon terminal Synapse Synaptic cleft 0 Space between presynaptic and postsynaptic neurons synaptic cleft o Synapsel whole thing Neurotransmitters 0 Chemicals that are released by the presynaptic neuron into the synaptic cleft to affect the postsynaptic neuron 0 Most are either excitatory or inhibitory 0 Figure 416 Amino Acids act as neurotransmitters n Glutamate Major excitatory neurotransmitter in the nervous system EPSPs n GABA Major inhibitory neurotransmitter in the nervous system lPSPs n Aspartate n Glycine Monoamines gure 415 n Synthesized from a single amino acid a Catecholamines synthesized from Tyrosene Dopamine o Controlling our muscle movements Norepinephrine o DopamineL DopaTyrosine precursors o Mood regulation Epinephrine o Adrenaline n lndolamine Synthesized from amino acid Tryptophan Serotonin 5HT 0 Mood regulation some antidepressants o Sleepappetite Acetylcholine 0 Created by adding an acetyl group to choHne 0 Released at the neuromuscular juncUon o Involved in learning and memoryattention keeps hippocampus working properly Alzheimer s Unconventional Neurotransmitters n Soluble gases 0 Pass through the membrane by osmosis into the next membrane Disappear very quickly hard to study 0 Nitric oxide carbon monoxide o Retrograde transmission Often produced by a postsynaptic ce go back and affect the presynaptic cell a Endocannabinoids Produced immediately before released 0 Can be produced in the dendrites fat soube molecules 0 Send a message to the presynaptic cell receptor Neuropeptides largemolecule neurotransmitters a String of 10 or less amino acids bigger protein a Endorphins endogenous opiates Receptor 0 Site on postsynaptic neuron on which neurotransmitters bond 0 Lock and key o If GABA is released and there are GABA receptors then GABA will have an effect Ligand 0 Any molecule that binds to another molecule 0 A neurotransmitter is a ligand for its receptor I Overview of Synaptic Transmission 0 Figure 46 IV Stages in Synaptic Transmission Neurotransmitter synthesis and storage make neurotransmitter o Manufactured in 2 ways In Axon terminal El Small neurotransmitter molecules are made in the cytoplasm of the axon terminal In a cell body a Large molecule neurotransmitters Neuropeptides n Made like all proteins are I Made in the cytoplasm of the cell body on ribosomes 0 Formation and storage in vesicles Small and large neurotransmitter molecules Made by the Golgi Apparatus Gather by synaptic membrane Quantum n the amount of neurotransmitter in each vesicle Vesicles have the same amount of neurotransmitter in them Increasedecrease the amount of quantum El El 0 Coexistence Some neurons can contain two neurotransmitters previously believed only one Only occurs with a small and large Release of neurotransmitter 0 AP opens voltagegated calcium channels Calcium comes in and causes the vesicles to spill their contents 0 Exocytosis The process of neurotransmitter release Calcium causes the synaptic vesicles to fuse with the presynaptic membrane Expel contents into synaptic cleft Figure 410 o Directed vs Nondirected synapses Directed n The site of neurotransmitter release and the site of action is close Nondirected n The site of neurotransmitter release and the site of action are not close 0 Activation of receptor site 0 lonotropic receptors Associated with ligandactivated ion channels Ligand Chemical that binds with something else Channels close depending on the presenceabsence of a Hgand Composed of a receptor binding site and an ion channel chemically gated The neurotransmitter does not ow through the receptor Action at receptor a Glutamate binds to receptor and sodium enters EPSP n GABA IPSP inhibitory GABA opens potassium and chloride channels Effects a Rapid about 10 milliseconds n Shortlasting n LocaHzed 0 Meta botropic receptors Associated with G proteins a GTP sensitive protein Composed of a receptor binding site and a signal protein linked to G protein Action at receptor a Can open ion channels a Activates the synthesis of a chemical called a second messenger n Affect signaling molecules inside the cell Effects a Not immediateslower n 30 milliseconds n Longlasting seconds minutes hours a Widespread and varied o Inhibitory and Excitatory Glutamate opens Sodium channels Electrical Chemical Electrical 0 Autoreceptors Located on presynaptic membrane Bind their neuron s own neurotransmitter Deactivation of neurotransmitter o Reuptake Neurotransmitter is taken back up into the presynaptic terminal to be used again Most neurotransmitters are deactivated this way Reuptake sites 0 Enzymatic Neurotransmitters are broken down in the synapse by action of enzymes Eg Acetylcholine V Gap Junctions sparkers weren t totally wrong after all Sparkers believed communication between cells were electrical Narrow spaces between adjacent neurons that are bridged by channels that contain cytoplasm Electrical signal can travel between these neurons 0 Very fast and goes in both directions Seems to be involved in synchronization of activity of neighboring neurons Vl Review 0 Seven steps in Neurotransmitter Action 0 Figure 417 Vll Drugs Agonistic vs Antagonistic Drug Effects 0 Figure 418 o Agonistic Make more neurotransmitter Parkinsons o Antagonistic lnhibit the effects of neurotransmitters Antipsychotics are dopamine receptor blockers Schizophrenia o l Structure of animal cells cells of the nervous system share features of other cells in the body 0 Figure 36 0 Cell Membrane O Separates inside of cell from outside of cell Two fat layers lipid bilayers 0 Small uncharged particles can ow through the fat in and out of the cell most things can t 0 Embedded in the membrane are proteins Signal proteins a Relays signals from outside of cell to inside of cell Channel proteins a Allow proteins to ow in and out n Charged particle has its own channel Particle Y ows through Y channel speci c to the particular ion charged particle n Sometimes open sometimes closed a Charged particles can only enterexit if they have a channel and if that channel is open 0 Nucleus Mitochondria o Powerhouse of the cell 0 Site of aerobicoxygen consuming energy Endoplasmic Reticulum Cytoplasm Ribosomes Golgi Complex Microtubules 0 ll Two kinds of cells in nervous system Neurons 0 Cells in the nervous system that receive and convey information 0 History Golgi and the reticularists n Anatomist argued that the neurosystem was like the circulatory system continuous stain a Golgi stain Ramon y Cajal and the Neuron Doctrine n Neurons are discrete individual cells that come very close together but don t touch a Communication between cells through this space a quotFather of Neurosciencequot a Used the Golgi stain to prove Golgi wrong 1906 Nobel Award Winners in Medicine and Physiology Late 1800s Golden Age of Neuroscience 0 Basic Structure Figure 35 Soma a Cell body Axon n Sends information a Axon coateras Neuron typically only has one but can have coateras where it branches off 0 Some are part of neurodegeneration but not all n Presynaptic terminals buttons bouton At the end of the axon Each button can communicate with the next neuron Dendrites n Neurons receive information from other neurons o Synapse El Dendritic spines Increase surface area of the dendrites More spines l more place for input Potentially thousands of places for input Some input goes directly to the cell body Come in all shapes and sizes 0 Certain ones are more stable than others 0 Learning and memory Spines change in number and shape all the time some stable some not Eg Estrogen increases dendritic spine density in hippocampus 0 Removed rats ovaries injected half with estrogen and counted spines 0 Signi cantly more with estrogen l does better on memory tests Stress induced changes in the number and shape of dendritic spines on mice hippocampal pyramidal neurons 0 Usually causes a reduction and also a different shape Easily modi able depending on external factors Gap between adjacent neurons where information is transferred from one neuron to the next 0 Myelin Sheath Fatty tissue that insulates many axons Increases the rate of neurotransmission If an axon has myelin l faster neurotransmission o Efferent vs Afferent Efferent Neuron that carries information away from a structure El O Glia 0000 O a All motor neurons Afferent n Neuron that carries information to a structure U Sensory neurons to the CNS Interneurons Neurons that axons and dendrites are all in one structure The whole neuron is in one structure Front cortex l Hippocampus afferent also has efference Reative to the part of the brain Very short axons Neuron that s entirely contained in one structure Variation See Figure Separate types of cells from neurons Do not transmit information based on our current knowledge More important than we used to think Role in synchronizing neural activity Housekeeping clean up waste and dead cells provide structural support 10x more in number than neurons neurons are 10x bigger take up the same amount of space in the brain Four types of glia cells Astrocytes a Star shaped n Synchronization w Arms synchronize the activity of neurons n Provide a supportive matrix for neurons Adheres to capillaries scaffolding in the nervous system Microglia n Respond to injury or disease a Surround the injured tissue and trigger an in ammatory response Ogliodendrocytes n Build myelin sheath in the Central Nervous System brain and spinal cord Schwann cells a Form myelin sheath in the Peripheral Nervous System 0 III Bloodbrain barrier Exists to protect the brain Prevents viruses and bacteria from crossing into the brain No gaps Some things can cross over 0 Fat soluble molecules l drugs of abuse 0 Small uncharged particles can cross charged cannot Hard to develop a chemo for brain cancer most things cannot cross this barrier o l Peripheral Nervous System Terms 0 Nerves Bundles of axons in Peripheral Nervous System white matter 0 Ganglia Group of cell bodies in Peripheral Nervous System gray matter no myelin Cranial and Spinal Nerves 0 Connect brain and spinal cord to the rest of the body 0 Cranial 12 pairs Direct connection to the brain Eg facial nerves attached to brain close proximity o Spinal Enter and exit the spinal cord through spaces between the vertebrae Mixed nerves afferent and efferent information sensory and motor Somatic Nervous System 0 Controls voluntary muscles and receives sensory information from muscles and skin 0 Sensory and motor information 0 Send information back to our brains about what we feel sensory feedback from our voluntary muscles 0 Efferent and Afferent information Autonomic Nervous System 0 Controls our glands and involuntary muscles heart Sympathetic n Arouses the organism U Release of epinephrine adrenaline n Fight or ight Parasympathetic n Quiets the organism n Decreases heart rate n Promotes digestion Appendix I n Twostage neural pathway In Parasympathetic rst stage long second short a Sympathetic rst stage short second long Arrangement of Ganglia n The ganglia in the sympathetic nervous system are located close to the spinal cord and lined up almost like a chain a Parasympathetic l ganglia are not linked 0 ll Central Nervous System brain and spinal cord Cerebral Spinal Fluid 0 Colorless uid that surrounds the brain and spinal cord 0 Provides a cushion and is protective Meninges 0 Brain and spinal cord are separated by the skull and the vertebrae by 3 membranes Dura mater n Outer most meninge n Isolates the CNS from other structures Arachnoid membrane a Next to dura mater n Looks like a spider web a Subarachnoid space Contains cerebral spinal uid Under arachnoid membrane Excess cerebral spinal uid is absorbed from this space 0 Not a meningesubcategory Pia mater n Delicate membrane that follows the contours of the brain precisely Anatomical terms referring to direction g 314 and 315 o Posterior Towards the tail Back of brain 0 Dorsal Towards the back Top of brain 0 Ventral Towards the stomach Bottom of brain 0 Anterior Towards the nose Front of brain towards forehead o Medial Towards middle 0 Lateral Away from middle 0 Sagital Anterior l Posterior Mid Sagital Cut l separates two hemispheres 0 Horizontal Plane Parallel to the horizon o Frontal PlaneCoronal Section 0 Cross Section 0 Terms 0 Tract A bundle of axons in the CNS white matter 0 Nucleus A cluster of cell bodies in the CNS gray matter Spinal Cord o Segmented each segment has sensory information coming in from the dorsal side and motor information going out on the ventral side Spinal Nerves n Pairs of nerves attached to the spinal cord at 31 different levels a Nerves peripheral nervous system I Made up of a ventral root and a dorsal root Ventral root motor efferent neurons carrying information away from the CNS cell body for these motor neurons is located inside the spinal cord Dorsal root 0 Dorsal root ganglia cell bodies of the dorsal roots bundle togetherjust outside of the spinal cord Central Canal a Space containing cerebral spinal uid a Spinal cord gray matter inside white matter outside lll Brain Features Overview o Gyri Bumps on the brain Sulci ssures Grooves on the brain Fissure really big sulcus More highly developed brains have more of both of these Ventricles 4 large internal spaces in the brain a Two lateral ventricles a Third ventricle a Fourth ventricle n Cerebral spinal uid ows throughout all connected Choroid Plexuses Network of capillaries that protrude into the ventricles from the Pia Mater Produce Cerebral Spinal Fluid White matter gray matter Brain gray matter outside white matter inside opposite of spinal cord Corpus Callosum Massive ber tract that connects the two hemispheres of the brain Anterior Commisure Small tract that connects the two hemispheres Cerebral Cortex Outer surface of our brain Subcortical regions Much subcortical area is made up of tracts Below cortex 0 Brief Overview of Brain Development 0 See Figures Hindbrain Myelencephalon and Metencephalon o Medulla o Pons Part of the brain Control of vital functions Damage to medulla dead or on life support Controls heart respiration Reticular formation a Group of about 100 nuclei that runs from the medulla up to the midbrain n Involved in sleep and consciousness Houses many of the ascending and descending tracts o Cerebellum Large structure with many folds at the back of the brain Involved with ne tuning of our motor movements balancecoordination Learned motor movements playing the piano Many GABA receptors alcohol hits the cerebellum quickly Midbrainmesencephaon o Tectum Roof of the midbrain Composed of two pairs of bumps n Inferior coicui bottom set Auditory function n Superior coicui top set 0 Visual function 0 Tegmentum ventral to the tectum Red nuclei n Involved in motor function Substantia nigra n Involved in motor function u Contains dopamineproducing cells that project to an area called the stratum When these cells are dying Parkinson s disease Forebrain o Largest region of the human brain 0 Diencephalon Thalamus a Large twolobe structure that sits on either side of the third ventricle n Comprised of about 20 nuclei cluster of cell bodies gray a Gateway for sensory information that s on its way to the cortex n Almost all sensory information from body brain goes through the thalamus Hypothalamus n Composed of about 22 small nuclei n Makes up about 3 of our brains I Involved in many behaviors Sex behavior appetite temperature regulation emotionshormone function sleeping Pituitary Gland 0 Attached to the base of the hypothalamus o Synthesizes and releases hormones in response to signals from the hypothalamus Optic chiasm 0 Located right on the inferior surface of the hypothalamus 0 Where axons from the optic nerve cross 0 Telencephalon Cerebralcortex El Cellular layers on the outer layers of the cerebral hemispheres Sensory information motor information complex thoughts processed 90 of the human cortex is referred to as neocortex 6layer cortex Major Fissures grooves Fig 324 0 Longitudinal ssure o Separates the two hemispheres Central ssure o Separates the frontal and parietal lobes Lateral ssure o Sits on top of the temporal lobe Lobes Occipital lobe o Processes visual information at the back of the brain 0 Primary visual cortex Very back part Visual information ends up here Damage to this cortical blindness no visual imagery can no longer imagine things in a visual way no dreams Parietal Lobe o Postcentral gyrus primary somatosensory cortex Receives somatosensory information from the body touch and feedback from the muscles where our body is 0 Temporal Lobe 0 Superior temporal gyrus primary auditory cortex Top of the temporal lobe Target for auditory information 0 Language Left side for most people 0 Other functions Helps recognize faces Processes complex visual information Frontal Lobe o Precentral gyrus Primary motor cortex 0 Prefrontal Cortex Most anterior part of the brain Executive function boss of the brain Higher level thinking Emotional regulation Limbic System subcortical structure a Form a ringcircle around the thalamus n Evolutionarily old a Hippocampus Involved in memory Lesion of the hippocampus cannot make new memories I Septum Cell bodies in the septum produce acetylcholine projected to hippocampus o Dying Alzheimer s n Fornix Fiber tract that connects a septum to the hippocampus Gray matter a Amygdala Involved in emotional regulation especially fear 0 When you re afraid and making a memory 911 a Cingulate Cortex Large strip of cortex just above the corpus Callosum Involved in affective behavior emotion Basal Ganglia subcortical structure a Amygdala n Striatum Caudate amp Putamen 0 Input center for the basal ganglia o Involved in motor movement 0 Controlling the force Parkinson s Disease n Globus Pallidus Striatum projects to this which then projects to the cortex Involved in Motor movement 0 Output center a Nucleus Accumbens Involved in rewarding affects 0 Chocolate sex drugs of abuse 0 0 TEST Know gure on page 73 o Midsagital section Don t have to know mamillary Identify lobes ssures o SAMPLE QUESTIONS When a neuron is at rest what isare attracting potassium ions to move out of the cell 0 A concentration gradient 0 An electrical gradient 0 The in ux of which of the following ions results in the release Concentration Gradient 0 Number of ions in the inside versus outside wherever there s more ows to less 0 Passive forces acting on 0 Voltage gated and Chemically gated ion channels ionotropic receptors 0 Action Potential Electrical chemical electrical Chemical release of neurotransmitter Dopamineproducing die Parkinson s o Acetylcholineproducing die Alzheimer s O o Cerebellum damage cerebral palsy Methods of recording activity in neurons 0 Intracellular recordings electrodes one in extracellular space one in cell body difference in charge 0 l Stages of Neurodevelopment Prenatal Development of Human Brain 0 Cells have to differentiate locate to appropriate sites and make appropriate functional connections How 0 Phase 1 lnduction of the Neural Plate 0 De nition of neural plate Embryonic cells have 3 layers from outer to inner ectoderm mesoderm endoderm A small patch of ectodermal tissue on the dorsal surface of the developing embryo First major stage of neurodevelopment in all vertebrae 0 Induction Process Seems to be induced from chemical signals from the mesoderm l outer layer that causes induction of neural plates 0 Totipotent multipotent cells Stem cells Totipotent cells have the ability to develop into any cell type in the body Weeks later l multipotent Multipotent neural cells can develop into any type of cell in the nervous system but can no longer develop into nonneural cells 0 Neural Plate to Neural Tube Neural plate l Neural groove l Neural Tube 0 Phase 2 Neural Proliferation o Proliferation increase greatly in number 0 Most of the cell division occurs in the ventricular zone 0 The differential sequence of proliferation between species is responsible for the pattern of swelling and folding that gives the brain of each species the characteristic shape o The pattern of proliferation is controlled by chemical signals from organizer areas of the neural tube 0 Phase 3 Neural Migration and Aggregation 0 Migration When cells are migrating they re in immature form no axons or dendrites formed yet Radial and tangential migration n Fig 92 n Radial straight line from ventricular zone to cell walls a Tangential occurs at parallel to the walls can go back or in a circle Two Methods n Somal translocation 0 Fig 93 Immature cell grows a temporary extension not an axon or dendrite to help with migration Attracted or repelled by chemical signal 0 Method can be used radially or tangentially n GliaMediated Migration Only used for radial A temporary network of glia cells called radial glia appear during development 0 Cells migrate along radial glia Timing is Everything I 6 layers of neocortex n Timing of proliferation and subsequent migration Neural Crest n A structure that is just dorsal to the neural tube a Formed from cells that break off from the neural tube a Will develop into the Peripheral Nervous System Neural tube is developing into CNS Chemicals guide migrating neurons by attracting or repelling them 0 Aggregation Get together form a structure once they get to where they belong Developing neurons that migrate to the same area form the structures Celladhesion molecules CAMs n Molecules located on the cell surface that have the ability to recognize and bind to CAMs on other cells n Mental retardation Gap Junctions n Many more in embryonic development than in postnatal a Way to connect cells that belong together 0 Phase 4 Axon Growth and Synapse Formation o Axon Growth Growth cone lopodia n Extends and contracts in ngerlike contractions a Chemical messengers a At the end of developing axonsdendrites n Searching for their destination Sperry s Classic Study a What guides axon growth In Experiment with frogs cut axons to see where they d grow I Took retina out and twisted it frog searching for the y in 180 degree mistake cut axons where would they grow back a Hypothesized they would grow straight grew back twisted n Concluded that there was a destiny for these axons place where they belonged and would go back to this place n Chemicals guide the location Updated view Direction may be guided by chemicals andor topographical arrangements 0 Synapse formation synaptogenesis Axons and dendrites have to know who will connect with who Occurs after our axons and dendrites are grown Research is behind axon growth Evidence that glia cells may play a role not entirely sure 0 Phase 5 Neuron Death and Synapse Rearrangement o Neuron Death Results from competition for lifepreserving chemicals ie neurotrophins supplied by their targets u If you have enough you live if not you die n Released by postsynaptic side that allows the presynaptic cells to survive knows how much is ideal How it is achieved a Originally thought to be a passive process a Necrosis Passive cell death necrotic cells break apart and spill their contents into the extracellular uid and cause harmful in ammation n Apoptosis The absence of certain neurotrophins triggers a genetic program inside the cell that causes the cell to quotcommit suicidequot Program causes cells to actively die Safer than necrosis Neatly packaged in membranes before the cell dies allows for microglia to come in and clean them up Problems with this cause cancer don t kill themselves when they should Neurogenative illness is when they kill themselves when they should not 0 Synapse Rearrangement Cell death lead to massive rearrangement of synaptic connchons O Focuses output of each neuron on a smaller number of postsynaptic cells thus increasing the selectivity of transmission ll Neurodevelopment Postnatal Postnatal growth of brain 0 O O 0 Brain volume quadruples from birth to adulthood Growth not due to development of new neurons except hippocampus and olfactory bulbs Neurons last a lifetime Growth thought to be due to Synaptogenesis n Differences in rate between brain areas 0 Primary visualauditory cortices maximum connections reached at about 78 months of age Prefrontal cortex maximum reached at about 2 years of age a Overproductionplasticity There are periods of synaptic loss that occur at different times in different brain areas before adult levels are reached Increased myelination n Increased white matter as we develop postnatally a Last area prefrontal cortex continues to build myelin until adolescence Increased dendritic branching gray matter 0 Development of cortical white matter vs gray matter White matter grows slowly and steadily until adulthood Gray matter growth is an inverted U Overproduction increase early on decrease to adult levels when gray level matter reaches adult levels that area is mature Development of Prefrontal Cortex 0 Functions Working memory a What you re working on at any giving moment Planning and carrying out sequences of actions Impulse control Following rules of behavior 0 Functional development and behavior perseveration Piaget after 7 months object permanence 0 III Effects of Experience in Early Development 0 Terms 0 Permissive Experiences Those that are necessary for information in genetic programs to be manifested Eg Language 0 lnstructive Experiences Those that contribute to the direction of development Eg Englishspeaking household develop English 0 Critical Period If it is absolutely necessary for an experience to occur during a time window in order for it to develop 0 Sensitive Period If an experience has a great effect on development when it occurs during a particular interval but it still can have weak effects outside that interval Eg Language development 0 General principle regarding effects of experience on development of neural circuits if neural circuits once formed are not used they do not survive and function 0 Effects of Environmental Enrichment and Deprivation Competitive nature of experience s in uence on neurodevelopment 0 Use it or lose it o How early experience can in uence organization of nervous system 0 During sensitive period of development auditory and visual areas rotated 23 degrees l tectum later rotated 23 degrees 0 Early music training in humans evidence that early intensive music training results in a greater area of the auditory cortex related to recognizing tones 0 Early piano playing increases myelination Mechanisms 0 Some evidence that experience in uences gene expression 0 IV Neuroplasticity in adulthood Not as plastic as a child s brain but the adult brain is still changing Adult neurogenesis 0 Making new neurons in the hippocampus 0 Evidence of neurogenesis in the olfactory bulb Cortical Reorganization o Rehab 0 Monkey experiment induced stroke right arm weakness tied good arm behind their back 0 Not to lose the area of the cortex 0 o l Skeletal Muscles Muscles that are attached to the bones By contracting them we produce movement Muscle Fibers 0 Each muscle is made up of individual muscle bers 0 Individual muscle bers controlled by axons 0 Typically a single axon innervates more than one muscle ber Eye one axon to every three muscle bers Leg one axon to every 100 muscle bers Action of Muscles Each muscle can only make one movement contraction In the absence of stimulation it relaxes Never moves in the opposite direction At joints muscles are arranged in opposing pairs Flexor Muscles n Bends the joint when it s contracted Extensor Muscles n Straightens the joint Antagonistic Muscles n Opposing sets of muscles ll Neural Control of Muscles Contraction Motor neurons Final common pathway 0 Muscles contract or not depending upon the message from motor neurons 0 Muscles act in a similar matter as postsynaptic neurons 0 Our muscles only move based on a message from these neurons NeuromuscularJunction 0 Where the motor neuron meets the muscle 0 Very ef cient to ensure that an action potential at the axon terminal will translate to a motor action 0 Acetylcholine Neurotransmitter used at the neuromuscular junction 0 Motorend plate The site on the muscle ber that is activated by acetylcholine 0 Muscle Twitch Each action potential arriving at the neuromuscular junction produces a single wave of contraction in the muscle ber called a muscle twitch OOOO Many muscle twitches l contraction The Motor Unit 0 One motor neuron and all the muscle bers that it innervates 0 Some are small some are large 0 Muscles that control delicate movements will have small motor units ngers muscles that need a lot of force have large motor units legs Contraction Speed Sprinter vs distance runner 0 Fast Muscle Fibers Produce quick contractions but fatigue quickly 0 Slow Muscle Fibers Produce slower contractions but have greater endurance maintain their contractions for longer periods of time Contraction force 0 Firing rate Adjust the ring rate of the motor neurons strong force of contraction higher ring rate 0 Recruitment Recruit more motor units the more you recruit the greater the force of the contraction Disorders of the neuromuscularjunction o Curare poisoning Poisoned darts common for hunting in South America Bind to the acetylcholine nicotinic receptors and block their function Antagonists at nicotinic receptors Prevents muscle twitches and contractions paralyzed o Myasthenia Gravis Muscle weakness Autoimmune disease in which the immune system is producing antibodies that are attacking the nicotinic receptors at the neuromuscularjunction Severity varies depending on where the antibodies are attacking Receptor Organs of Tendons amp Muscles o Golgi Tendon Organs Sensory receptors located in the tendons connect muscle to bone Provide feedback regarding muscle tension 0 Muscle Spindles Give feedback regarding the length of the muscle Re exive Movements 0 De nition An automatic involuntary response to a stimulus When a sensory event translates into a motor action 0 Example stretch re ex A brief strong contraction of a muscle that is temporarily lengthened Kneejerk re ex Adaptive function u Allows us to keep external forces from altering the intended position of the body lll Brain Motor Systems Pyramidal Motor System 0 Composed of pathways that originate in the cerebral cortex and project to the spinal cord 0 Direct control of motor movement 0 Initiates the movement Extrapyramidal Motor System 0 Motor systems in the brain outside the pyramidal system 0 Helps to control movement by communicating back and forth with the pyramidal system IV Sensorimotor Association Areas Posterior Parietal Association Cortex amp Dorsolateral Prefrontal Association Cortex 0 Functions Before we can move we have to get information about our body status as well as the status of external stimuli V Pyramidal System 0 Starts in the cortex and projects to the spinal cord Cortex 0 Secondary Motor Cortex Function n Active during the planning of movement a Smooth sequence of events Premotor cortex amp supplementary motor cortex Inputs and Outputs 0 Primary Motor Cortex The major point of departure of motor signals Electrical stimulation can elicit movement Adjacent areas in your body have adjacent areas in your brain that control them The amount of primary motor cortex devoted to control of an area is related to its precision Connections from cortex to spinal cord motor pathways 0 Dorsolateral Tracts control movements of the periphery limbs contralateral side left side of brain controls right side limbs Dorsolateral cotricospinal tract direct a Direct tract from the cortex to the spinal cord Dorsolateral Corticorubrospinal tract indirect n Cortex to the red nucleus to the spinal cord o Ventromedial Tracts Ventromedial Cotricospinal Tract direct Ventromedial Corticobrainstemspinal tract indirect Motor Effects of Cortical Damage 0 Hempilegia Loss of voluntary movement in one side of the body Usually result of damage to the motor cortex 0 Apraxia Speci c loss of skilled voluntary movement Damage isn t always in the motor area various areas of the cortex 0 Contralateral neglect Disturbance of a person s ability to respond to stimuli on the opposite side of the body Vl Extrapyramidal Systems In uences movement indirectly by communicating back and forth with the pyramidal system Basal Ganglia o Helps us control our movement force 0 Caudate and Putamen Collectively called the striatum Input centers of the basal ganglia n Receives input dopamine from the substantia nigra o Globus Pallidus Output area of the basal ganglia Sends information to the thalamus which projects to the cortex 0 Disorders Parkinson s Disease a Result of deteroriation of dopamine producing cells in the substantia nigra Huntington s Disease a Genetic disorder a Starts off in the basal ganglia initial areas effected Tourette s Syndrome n Disorder where the brain disruptions are in the basalgangHa n Damageabnormalities n Often lessens with age a Too much excitation getting to the motor cortex Cerebellum 0 Inputs Receives information from both the primary and secondary motor cortices 0 Function Communicates back and forth with the areas of the motor cortex to control motor movement Timing and precision of motor movement Learned motor responses piano playing 0 l Lateralization The behavioral and cognitive abilites that each hemisphere specializes in II Hemispheric Connections 0 Corpus Callosum o The main connection between the two hemispheres bundle of axons lll Visual Connections to Hemispheres Right amp Left Visual Fields 0 Right Visual Field projects onto the left side of the retina on each eye 0 Left visual eld projects onto the right side of the retina on each eye 0 R Visual Field L half of each retina l L Hemisphere o L Visual Field R half of each retina l R hemisphere Optic Chiasm 0 Most information travels back and forth immediately after it arnves 0 IV Auditory Connections to the Hemispheres Each ear primarily receives information from one side Help us localize where the sound is coming from Each ear has connections to both hemispheres Connections to the contra lateral side are a little stronger 0 V Split Brain Research General Behavior 0 Severe seizure disorders don t respond to drugs respond to severing of the corpus callosum 0 Has little effect on people Experiments 0 Stare at X in middle 0 Picture in left eld house right visual field right hemisphere 0 Can t tell you what they saw right hemisphere 0 Spoon in right hand can say what it is spoon in left hand can t 0 Spoon in left visual field pick up with left hand l going to right brain l cannot identify 0 VI Hemispheric Specialization Table 161 0 VII Language Dominance Process language on left side 0 And Handedness o 90 of people are born righthanded 0 Of the righthanders 96 are leftlanguage dominant 4 are rightlanguage dominant very few righthanders have mixed language dominance o 10 lefthanded 7O are still leftlanguage dominant 15 are rightlanguage dominant 15 have mixed dominance and American Sign Language 0 Your rst language is American sign language follows the same pattern as spoken language 0 Brain damage on the left side impaired in American Sign Language 0 Testing for Language Dominance Wada Test I Find out where your language area is n Anesthetize parts of the brain and ask questions Dichotic Listening Tasks n Send two different numbers at the same time to each ear what did you hear u Left language dominant more often report what s heard in the right ear I Not as accurate Functional Brain Imaging n Cognitive tests and see what areas of the brain are activated El 0 l Paul Broca and Tan 0 First behavior based function that was found to be localized Broca and his patient Tan Lesion in the frontal lobe Broca s area 0 ll Hierarchal Structure of Language Phonemes 0 Basic speech sounds of any language Morphemes o Smallest linguistic units that carry meaning 0 Root words pre xes suf xes Syntax 0 Grammar rules of the language 0 What combination of words are permitted in a language Semantics o How our language expresses meaning 0 III Localization of Language in the Brain Traditional View Broca s area frontal operculum o Looked at where Tun s damage was that s where speech lies 0 Contains the articulation pattern that your motor areas need to form words 0 Sends the program to the motor cortex so you can talk Wernicke s Area planum temporale 0 Patients with severe comprehension de cits 0 Temporal lobe behind the primary auditory cortex 0 Thought to contain the meaning of words Arcuate Fasciculus 0 Fiber tract that connects Broca s and Wernicke s area Angular Gyrus 0 Behind Wernicke s area 0 Proposed to be involved in reading 0 O Linguistic meaning is given to the written word IV The WernickeGeschwind Model of Language Fig 1611 0 V Disorders of Language Broca s Aphasia 0 0000 Acquired Aphasia head injury or stroke Receptive Aphasia vs Expressive Aphasia Broca s Expressive Impaired language production Effortful and slow speech Problems at the phonemic level Effect on syntax Have content words but tend to leave out the function words telegraphic speechquot Eg I want to go home Go home Effect on Comprehension Subtle dif culties in comprehension The boy chases the girlquot understood The girl is chased by the boyquot more confusing Wernicke s Aphasia O 00 Trouble at the semantic level in general everything else is OK morphemic syntactic graphemic etc Effortless and uid speech ln ection grammar good speech makes no sense Someone that doesn t know the language wouldn t be able to tell o Vocabulary words and function words 0 Effect on comprehension have trouble 0 Global Aphasia o All language is lost production reception ability to speak read write 0 Still can take care of yourself Anomic Aphasia 0 When you can t nd the right words 0 Trouble coming up with the names of things Vl Criticism of the WernickeGeschwind Model 0 Way too simplistic Surgical removal of cortical tissue 0 Evidence Wernicke and Geschwind used 0 Most evidence indicates that if you have a removed Broca s area there will be few longlasting de cits o Supporters of WG model response Dismissed this criticism 0 Brain Damage 0 Size of lesion is important Small discrete lesions in Broca s area seldom produce lasting language de cits Mediumlarge lesions can produce language de cits o Anterior vs Posterior Damage More anterior more likely to have articulation de cits More posterior all other language de cits more likely to occur 0 CT and MRI scans o Anterior vs Posterior Damage Living patients with brain damage earlier were only autopsies Patterns remained consistent Discrete damage limited to Broca sWernicke s area did not cause the predicted problems 0 Right hemispheric damage rarely results in language disorder for left language dominant patients 0 VII Current status of the WernickeGeschwind Model 0 Used in clinical practice to base diagnoses on 0 Current researchers do not generally use this model 0 Empirical evidence supporting two elements 0 Areas around Broca sWernicke s area probably play some role in language not the all encompassing role the model predicted No support for speci c predictions 0 Discrete damage to these areas rarely cause severe language de cts 0 Brain damage outside of these areas can cause language de cts o Aphasias rarely exist in the pure forms like Broca s or Wernicke s o A lot of individual differences the more complex a behavior usually the more individual differences exist Vlll Cognitive Neuroscience Approach to Language Premise Activity in brain areas for speci c cognitive processes pg 416 o Underlie languagerelated behaviors Eg phonemic level underlies language but very different from vocabulary knowledge Different areas of the brain that probably process all these different functions 0 Have functions independent of language 0 Are likely to be small widely distributed and specialized Methodology 0 Approach the study in healthy patients 0 o De nition Refers to a particular kind of subjective feeling that is aroused by objects or events that can be real or imagined that have high signi cance to the individual ll Three components of emotions Feeling or subjective conscious experience cognitive component 0 Pattern of physiological arousal changes associated with visceral organs 0 Pattern of overt expression behavioral lll Subjective Conscious Experience Classifying Emotions 0 Different scales 0 Brain areas involved 0 Frontal lobe is crucial for generating the conscious experience of emotion o Amygdala assess the emotional signi cance of stimuli particularly but not necessarily exclusively fear and anger Auditory fear conditioning procedure a Rat in a cage not afraid a Pair stimulus music conditioned stimulus with a shock naturally afraid unconditioned stimulus I Learned fear Auditory fear conditioning neuroanatomy a Direct connection between Medial geniculate nucleus and amygdala n Medial Geniculate Nucleus only simple tones n Fig 179 o Lateralization of emotion Smile on the left side of the face rst right side has emotions previously thought More bilateral than previously thought 0 Individual differences in the neural mechanisms of emotion The more complex a behavioral function the more individual differences across subjects 0 IV Physiological Arousal Theories of Emotion o Commonsense Theory Perception of bear l Feeling of fear l Physiological reactions 0 JamesLange Theory Perception of bear l Physiological reactions l Feeling of fear Relationship between spinal cord lesions and emotionality a Report less intense emotions related to where the injury was 0 CannonBard Theory Perception of bear l separate informs both feeling of fear and physiological reactions parallel 0 Modern Theory Everything informs everything Circular model Schachter and Singer experiment a Experimental group all got a shot of adrenaline epinephrine I Put the people in a room with a mildly rude person a Half were not told what shot they got attributed it to mildly rude person more likely to get in a ght D Other group told didn t respond to mildly rude person a Physiological reaction intensi ed emotional response Mechanisms of Physiological Arousal o Limbic System Previously thought to be the quotemotional systemquot 0 Brain perceives emotional event and activates Hypothalamuspituitaryadrenal cortex HPA axis releases glucocorticoids stress hormones involved in strong emotional response Sympathetic nervous system 0 V Expression of Emotions Facial Expressions 0 Darwin Facial expressions were used prior to language to signal to others how you were feeling predict behavior 0 Six basic expressions Fig 175 Facial Feedback Hypothesis 0 Does behavioral expression affect other aspects 0 Pen between teeth or lips smilelook angry 0 Shown happiness and angerinducing slides smile affected decisions 0 Voluntary Control of Facial Expression 0 Duchenne smile real smile Orbicularis oculi pulls your eyes up for real smile involuntary Zygomaticus major pulls your lips up voluntary o Facial electromyography EMG studies Micromovements will appear hard to fully block emotional response 0 What is it o A nonspeci c response of the body to demands placed on it 0 ll Physiological Response to Stress Stressor is received by brain Neural pathways activate hypothalamus Hypothalamus activates two systems HPA axis and sympathetic nervous system 0 Hypothalamus acts on anterior pituitary to reaeaase the hormone adrenocorticotropic hormone ACTH into bloodstream o ACTH acts on the adrenal cortex to cause release of glucocorticoids main one is cortisol Measure of cortisol levels most common physiological measure of stress 0 Glucocorticoids are carried via blood throughout body and will act on organs and muscles 0 Sympathetic division of the autonomic nervous system Increased heart rate elevated blood pressure dilated pupil etc Increased release of epinephrine and norepinephrine from adrenal medulla 0 III Adaptability of Stress Response 0 Variety of stressors elicit a relatively consistent set of responses 0 Why 0 Need to mobilize energy energy storage is inhibited and existing stores of energy are broken down to be readily usable o Curtail nonessential physiological processes Digestion reproduction excretory system 0 Blunt pain and in ammation Eg Someone breaks their leg and can still run away endorphin release by sympathetic nervous system endogenous opiates 0 IV When Stress Response Becomes Maladaptive Prolonged activation 0 When not activated for a physiological reason 0 Eg Prolonged emotional stress 0 V Stress and Health 0 Brief activation of stress systemsquot enables the body to deal with stressors Chronic activation can result in health problems 0 Gastric Ulcers O Beginning in 19505 scientists attributed ulcers to stress a Animal studies a Proposed mechanism 0 When you re under prolonged stress digestive system is not working properly when you do eat stomach rebounds and ulcers form ln 19805 ulcers attributed to bacteria H pylori n Evidence o If you give a person antibody it will x the ulcer 95 that had ulcers also had this bacteria In Problems 0 70 of people without ulcers also have the bacteria Current thinking is that ulcers result of combination of bacteria and stress and certain drugs like ibuprofen o Psychoneuroimmunology study of interactions among psychological factors the nervous system and the immune system Brief stress boosts immune response Prolonged stress harmful General rule Stress rarely makes you sick Chronic stress can worsen a preexisting condition or can lower your defenses to make you more susceptible to illness 0 Effects of stress on cognition o YerkesDodson curve There s an optimal level of arousal that s ideal to learnmake a good memory Figure 144 o Mechanism Hippocampus has high levels of corticosteroid receptors glucocorticoid a Short term activation helpful a Chronic or extremely high levels of stressrelated activation harmful a Role of Type I and II corticosteroid receptors 0 Figure 146 0 Chronic activation of corticosteroid receptors results in damage to hippocampal cells thought to be reversible if stress subsides and negatives effects on hippocampus dependent learning and memory I Terms A Learning the acquisition of information as a function of experience resulting in a relatively permanent change in behavior or behavioral repertoire o B Memory Stored information produced by learning 0 C Encoding The placing of new information into memory 0 D Consolidation Moving short term memories into long term memory 0 Not all short term memory is strengthened into long term memory 0 E Retrieval accessing stored memories 0 0 ll Types of Memory 0 A Shortterm memory memory for event that have just occurred 0 Limited 7 items give or take two 0 You can chunk them group them to remember more 0 Once an item is lost from the short term memory store its likely gone forever OOOOO o B Longterm memory Moving short term memories into long term memory 0 Not all short term memory is strengthened into long term memory 0 LIMITLESS 0 We think these memories can last inde nitely 0 We think that we have more stuff up there than we can imagine that its just a problem with retrieving it all 0 C Working memory Anything you re working on at this very moment 0 Prefrontal cortex dependent working memory 0 Combination of acquisition encording retrieval short term memory long term ect o D Declarative or explicit memory 1 semantic declarative memory 0 Memory of general facts concepts and knowledge 0 Cant tie it to a particular experience but knowledge gathered by just knowing 0 memory of knowingquot 2 episodic declarative memory 0 Personal memory for event in your past 0 E Nondeclarative or implicit memory Defn All memories that not declarative o The in uence of recent experience on behavior even if you don t realize you re making a memory Skill learning often falls in this I Types of Learning A Nonassociative learning only a single stimulus or environmental event is involved OOOO o 1 Habituation when an organism learns of a repeated exposure of a stimulus to ignore it ignoring a train when you live by it 0 its a survival mechanism 0 still a type of learning 0 2 Sensitization an increase in response to a mild stimulus as a result of previous exposure to more intense stimulus an organism on high alert 0 B Associative learning Learning a relationship between two stimuli or between a stimulus and behavior allows us to learn causal relationships in the world 0 1 Classical conditioning the tone to scare the shit out of the rat pairing UCS to UCR making it into a CS to a CR 0 2 Operant conditioning Response is followed by reinforcement increases probability of responding or punishment decreases probability of responding o o The search for the engram 0 Karl Lashlsy 18901958 cartissl knife cuts mads by Lsshlsy39 its disrupt Issrnsd sssscistisns O trained the rats and then lesion a part of the brain that he thought would be responsible for it he could not localize a single spot for memory the more the cuts he did the worse it got but he probably fucked up a lot of stuff he concluded that there is no place in the brain that is more important for memory than others 0 there is no location for memory in the brain that is more important than other places 0 IV The Role of the Hippocampus Cut out parts of the medial temporal lobe His epilepsy was a result of a head injury he was able to go to high school but it got worse Result of the surgery devastating memory de cit The surgery took his hippocampus The most studied case Henry Gustav Molaison His dad was a cajun WOO Clean lesion of the hippocampus but theres no way now to get a clean lesion of the hippocampus o A The case of HM o 1 Learning and memory skills impaired he had extreme de cits in the ability to make new memories 0 watch the movie momento o it prevented short term declarative memories from becoming long term memories 0 if you had an accident and only hurt your hippocampus you would be able to remember you and your parents and your childhood but you couldn t make new declarative memories from then on 0 Makes other guys research wrong hippocampus is very important in making memories 0 There are other things outside the hippocampus that are important for memory learned from the things that HM COULD do 2 Learning and memory skills spared a shortterm memory b remote memory c skill learning d some forms of classical conditioning B Hippocampus and declarative memory 1 Delayed matchingtosample and delayed matchingtononsample tasks 2 Spatial memory a radial maze b Morris water maze OOOOOOOOOOOO 3 Memory consolidation Flo lawi labE i Cl a nr bub m Tar 3quot ng own hlasm quot H mf rl Ma y FIG 111 aw 1wcally H d W1 ma lalvnemporall Henw Gustav Malaisan HQquot M Eliiii39lk39l39 i l39 HI l ll 39l39 ll Illl l la fl i In ll H39ii l39l w x m u quotFill H39li39i il liiuli Lecture 032415 Learning and Memory Terms 0 The acquisition of information as a function of experience resulting in a relatively permanent change in behaviour or behavioural repertoire o Stored information produced by learning 0 Three stages encoding consolidation anol retrieval 0 The placing of new information into memory 0 Moving shortterm memories into longterm memory store Retrieval o Accessing stored memories Types of Memory ShortTerm Memory Memory for events that have just occurred Limited storade Once an item is lost from STM it s gone forever unless it s been moved to LTM LongTerm Memory Limitless Memories can last inde nitely We have more things in LTM than we re aware of 0 May have to do with difficulty retrieving information o Retrieval becomes more difficult over lifespan Working Memory Lots of different de nitions Dependent on prefrontal cortex Combination of shortterm and longterm memory Anything being worked on at this very moment 0 Comparing what is being said STM to what one already knows LTM 0 Includes acquisition encoding and retrieval Declarative or Explicit Memory conscious long term memories Declarative memory is the more common term now explicit means same thing Refers to things that one can bring to mind and explicitly declare Ex how old are you What did you do last night What s the hippocampus Semantic declarative memory 0 Memory of general facts concepts and knowledge 0 Don t always know where the information came from 0 Sometimes called the quotmemory of knowingquot 0 Ex where s the Eiffel tower Episodic declarative memory 0 Personal memory for events in one s past Not clearcut some things overlap between semantic and episodic Nondecarative or Implicit Memory subconscious long term memories All memories that are not declarative In uence of recent experience on behaviour even if one doesn t realize they re making a memory Skill learning often falls into this Types of Learning Nonassociative Learning Only a single stimulus or environmental event is involved Simple kinds of learning help test animal models Habhua on 0 When an organism learns over repeated exposure to a stimulus to ignore it 0 Survival mechanism pay attention to a novel stimulus ignore repeated stimuli 0 Ex move a block away from a train track rst night very difficult sleeping after living there for a few months you don t even notice it Sensitization o Opposite of habituation 0 An increase in response to a mild stimulus as a result of previous exposure to more intense stimulus 0 When an organism is on high alert 0 Ex if you live on Broadway in an old house every time a truck goes by your house vibrates when in California you get caught in an earthquake when the same stimulus happens again on Broadway you jump Associative Learning Learning a relationship between two stimuli or between a stimulus and a behaviour Helps us learn causal relationships in our world Classicalconditioning 0 Every time a rat hears a tone it gets shocked and jumps up after a while it jumps in response to the tone without the shock o Unconditioned stimulus automatically fearful stimulus shock o Conditioned stimulus something that was previously not scary tone but has become scary after being paired with the UCS Operant conditioning 0 When a response is followed by reinforcement or punishment 0 Reinforcement anything that increases future probability of responding o Punishment anything that decreases future probability of responding The Search for the Engram Attempting to discover where memory was in the brain Trained rats on a maze lesion the cortex of the rats brain see if the rat would remember the maze Made hundreds of cuts but never found the place where memory was localized Eventually found there is no place in the brain that is more important for memory than other areas The Role of the Hippocampus The Case of HM quot1Pquot quot 5 39IquotIquotI I 39IF 39 3 399 III 394 LI iI39 IIl39 HIMml quotl39l rally ilu IIIl 39I39iIrLi I lII39i I 39 I39iHIJ I39illlii l39f Ii39 III39I39IIIiIIII IiI rihi III III lilun nl39lquotl39llllll39l i quotll lllllrlu39 39I 39 I 39l 39a l39u Il39 39IiII 39 III ral IIHII IIr IIL 39lquot39i39quot IIIIEI IIIAII villfn F1 l39 nil laquot inille39Flll III illl quota mullill 39I EII39 I u39ill I39ll Ilil39 IIIIJ Iifiulilll lin IIIHIIII3939 I in A man in early 205 with severe seizure disorder uncured by drugs 0 Couldn t function 0 Epilepsy a result of an accident on his bike when he was young People knew at the time that MTL structures were related to epHepsy 0 They gave him a medial temporal lobectomy successfully cured it o This removed his hippocampus As a result of the surgery he had a huge memory de cit He was the most studied neurological patient in the history of neuroscience Learning and Memory Skils Impaired Extreme de cit in ability to make new declarative memories 0 Prevented shortterm declarative memories from becoming longterm ones 0 Remember everyone he already knew couldn t remember new people or things Found out that Carl Lashley was wrong the hippocampus is very important for memory The Role of the Hippocampus The Case of HM Learning and memory skills spared o Hippocampus is probably not involved in all spared domains 0 Shortterm memory 0 Remote memory able to remember things from a long time ago eg parents house he grew up in etc o Skill learning could learn many things despite having no recollection of having learned them Things he learned with lots of practice may have eventually been taken over by other areas Ex star drawing task turntable task Implicit skill learning 0 Priming when previous exposure to a stimuli even if unconscious affects subsequent responses 0 Ex exposed to some stimuli then asked to ll in the blank 0 Ex incomplete pictures task 0 HM had no conscious recollection of what pictures he saw but he still got quicker at identifying the picture 0 Some forms of classical conditioning Hippocampus is a bilateral structure People interested in BampB would remove hippocampus in different species and see what they could and couldn t do each petal nmpimap mumamt Broraw HMnin ma inn 0 A good animal model would parallel human abilitynonability 3 39l hour In 5511 Sat 2 Sat 3 Sat 4 Gal 3 a quotk i vquot quot 1 397 l 5 39 I l I 2 lniliul Halest I am 1 SEN Sat 2 Hippocampus and Declarative Memory 1 H Delayed matchingtosample and i delayed nonmatchingtosample 3 quot 0 Train monkey to either look quot 4 E nial 3quot 7 E under blue disk or pyramid for food 0 Monkey moves a blue disk to get food from underneath it 0 Then there is a delay this is where memory kicks in monkey has to remember quotblue diskquot 0 Monkey is given a choice do you want to look under the blue disk or the pyramid Matchingtosample monkey will look under blue Numbernil MirrorDrawing Ermra bl HEM m1 Each Tria E j L I disk Nonmatchingtosample monkey will look under pyramid o This is the typical task goes against their tendency o Investigated how delay time affected performance in normal controls and HClesioned monkeys When the delay was 8 seconds both groups performed similarly At 15 seconds HClesioned monkeys were signi cantly impaired Number of correct trials continued to decrease over time85gt155gt1mgt10m Even controls got worse over time but less than HC lesioned Medial temporal lobe lesions i Normal controls 100 1 ins U I I d 7 7 i ex 1 quot O Q j A screen is lowered Fr 7 7 7 i 2 in front of the monkey C during the delay period 3 L 39 I D 39 2 39 39 B Hn 9 m unfamiliar obje Retention Delay Iii 39 co 33 p399 b ec j 8 8 seconds 15 seconds 1 minute 10 minutes a FTT i The monkey musl i i 39 remember the sample obiect and then select the unfamiliar object to obtain the food beneath it o Shuttlebox in rodents Food placed under orange block on right side of box Then have to go to the opposite side and nd the food Matchingtosample nd it under orange block 0 Nonmatchingtosample nd it under green triangle Similar pattern with rats short delay means no impairment for HCIesioned rats longer delay more impairment I 7 Tha gamble ahjam la peatad mixer tine 1am cup al time and an anjaafl mammal 1 ins aarr39qala nhlan i and a naval nhianl arrL planed ne39er lhe lwn Mimi hupa al1ha olhar amt Fund cup II II Sample T H When 1ha gliding mar la raised rampaging 39ll IEl 3am animal a 1ralhad1nnd izsaprlua ra39l rum 63min in lira aai39mla and pamhaa II 39 i rTl39lEi1 a palace 1 load la epn iled In a l39nnrlElnl iary Au madmrism lnl39o ma amplan I39mell aura Fmd 7 Tha aaimll nhjam i3 mqim aialy rmn uan my inn amparlimmar ma ral mmalna al ma m and of ma Mui nhy Em Lintll Eha pmmrm delay pariml la mar lag 1 maul9 Than Ina ulnar l n39r Ea ralisla in expnae lhe lwa nhenla at tha rather and 39l ralnad ram remamhar ing lhelr prmluua mullhlar th iha sai sse nlJac5i run in 1hn novel nhenl andpuahitaaida1nd 1mm i slammed lift IM amused nilp The aliding dam at than miner and la IMMM behind me rail i Tim rm 1hah rum in lha carrier or in liilurr tar39ji hm aml Ina clnn is claimed Llahlnd Then new lms am r39r thlEl 39lai tha heal 1rlal amanlaga al lha Mun iby hm ES 39ihal39 Ina l39a39i I39JIII m1 Iii L Ila Eler I dining nr halwaan iilala Spatial memory 0 Radial maze Put rat in the middle of the maze and food rewards at the end of each arm Task eat the food and remember where they just ate Rats natural tendency is not to return to a place where they just ate Smart rat will travel to all eight arms and then quit Dumb rat will travel to a few then start randomly looking in all of them Damaging the HC causes impairment on this task can t remember where they ve gone LTM task 0 Only four of the arms have food in them 0 A normal rat will after several trials never go into the arm that doesn t have food in it STM error eating the food from one arm then going back into it afterwards to get food LTM error going into an arm that never had food 0 Morris water maze Water is milky and opaque There s a hidden platform under the water 0 Rats don t like being in water will look for a way to get out If they develop spatial memory over trials they will begin swimming straight to the platform rather than looking around Memory consolidation 0 HM was missing this had STM but couldn t move it to LTM o This is what the hippocampus does allows us to consolidate shortterm memory into longterm memory Test given before ECS Test given after E08 60 39 50 r 8 9 1 3 4 5 6 7 Memory percent of TV show titles correctly recognized Retrograde AmneSIa 10 1 7 years years years years years number of years before ECS that oneseason TV shows played Duration of Learning ECS Interval Storage of LongTerm Memories LTMs are stored all over the cortex They go back to the original place where they came in 0 Ex if you have a memory of your grandfather you will remember his smell touch look etc all the sensory systems are involved Difficult to knock out all longterm memory 0 Memory may be a little fuzzy but difficult to get rid of all of it Fullblown LTM is made up of strengthened connections between all of these areas Unsure of how long consolidation takes could be days months or even years LTM is mostly independent of the hippocampus Nonhippocampal Memory Systems There are learning and memory processes independent of the hippocampus as demonstrated by HM 0 These are called nondeclarative memories Striatum and Procedural Memory Explanation 0 Procedural memory habits and skills built into our motor system don t have to be exclusively motor Most tasks that HM could do involved procedural memory 0 Mostly unconscious Example 0 When you drive to a new location hippocampus tells you what to do 0 When you drive to work everyday for a year striatum takes over habit Example of how to test Tmaze 0 Train rodents to nd food on right side of T o What did the rat learn Food is in the NW corner of the room hippocampus Food is there when I take a right striatum o Rotate the Tmaze If the rat nds the food anyway hippocampus If the rat just turns right striatum After 10 trials most use spatial cues 0 After more than 10 trials they use habit Similar to humans use HC at rst then use striatum habit Estrogen and Hippocampus Estrogen has positive effects on the hippocampus o Estrogen increases dendritic spines in hippocampus 0 Thus injecting estrogen will bias the organism to use the hippocampus over other systems whether or not that s adap ve Memory systems can compete for control Hippocampaldependent vs striataldependent memory tasks 0 Place learning learn where the food spatially is located 0 Response learning learn to always turn right to get the food 0 Estrogen enhances performance on place learning but impairs performance on response learning Thus estrogen enhances performance on tasks in which it s advantageous to use the hippocampus and impairs performance on tasks that depend on the procedural memory system Am ygdaa and Emotional Memory Explanation o Emotional memory recalling events coupled with the physiological response that was present when the event occurred Example 0 Get in an elevator with a woman who has perfume on 0 Start feeling good unsure why 0 0 Remember that it s the same perfume that my high school girlfriend used to wear at this point it becomes a declarative memory Example of how to test fear conditioning 0 Following the pairing of a neutral stimulus with an aversive stimulus the neutral stimulus elicits the cluster of behaviours related to fear state Giving a rat a shock in the right side of a shuttlebox o Eventually will avoid the right side because they remember getting shocked there 0 Overview of Current View of Multiple Memory Systems Declarative memory gt hippocampus gt go back to areas where it was formed Procedural memory gt striatum gt go back to areas where it was formed 0 Cerebellum is also involved in this type of memory Emotional memory gt amygdala gt go back to areas where it was formed These different systems consolidate these types of memories then go elsewhere for storage These areas are mostly association cortices Double Dissociation Experiments Evidence for MMS Examples of Human Studies Double dissociation always includes three groups two with de cits in appropriate brain areas and one control group 0 Parkinson s patients have dysfunctional striatums 0 Early Alzheimer s patients have dysfunctional hippocampuses 0 Normal controls for comparison Two tasks one hypothesized to be dependent on striatum other dependent on hippocampus o Incomplete pictures task striatum 0 Can you name some of the pictures you saw Were you working with a man or a woman hippocampus Resu s 0 Controls do well on incomplete pictures task and able to answer questions 0 Parkinson s impaired on incomplete pictures well on recall questions 0 Alzheimer s well on incomplete pictures impaired on recall questions Unfortunately Parkinson s patients have motor problems above and beyond striatum damage don t want to confuse this with learning so don t use a motor task Examples of Animal Studies Amnesia Anterograde Amnesia A loss of memory for information acquired after the injury or surgery This is most likely to happen after a head injury Retrograde Amnesia A loss of memory for information acquired before the injury or surgery 0 Rare to have pure retrograde amnesia Temporally graded retrograde amnesia o Happens with hippocampal damage 0 Losing what happened immediately before injury or surgery 0 Occurs with STM that hadn t yet been consolidated to LTM Amnesia A loss of memory particularly declarative memory Anterograde Amnesia A loss of memory for events that happened after the brain damage Retrograde Amnesia A loss of memory for events that happened before the brain damage Temporally graded retrograde amnesia 0 Based on time happens for anterograde amnesia 0 Memories occurring shortly before the brain damage are lost 0 Those memories that hadn t turned into LTM yet hadn t consolidated yet Understanding Amnesia Role of the Hippocampus Hippocampus converts STM to LTM and helps us form new declarative memories Anterograde amnesia with hippocampus damage new memories never become longterm so one can t remember anything after the damage Electroconvulsive shock therapy ECS 0 Last ditch effort when a patient is depressed and nothing else works 0 ECS induces some amnesia including temporally graded retrograde amnesia o Looked at TV shows that only played for one season asked participants about these shows Asked them questions about TV shows prior to ECS and after ECS o ECS had no effect on TV shows before ECS but signi cantly affected the number of questions they could answer about TV shows that came out 13 years before surgery after they underwent ECS Alzheimer s Disease Most common cause of amnesia Affects 7 of people over 65 about 50 of people over 80 Brain Abnormalities Accumulation of abnormal form of tau protein 0 We all have the normal form of tau protein it forms the cytoskeleton structural component of neurons 0 The abnormal form of protein is dysfunctional Cytoskeleton no longer works Cell starts to die 0 Neuro brillary tangles accumulate Leftover mess from abnormal tau protein 0 Impaired function and eventual death of neuron Extracellular deposits of amyloid form senile plaques 0 We all have amyloid precursor protein 0 For most of us the precursor protein is cleaved broken into a harmless form of amyloid that is taken up and dissolved Don t know what the function of this protein is but it is harmless o In AD the precursor protein is cleaved into a toxic form that can t be taken up and dissolved o This toxic protein accumulates between neurons so the communication is disrupted A lot of these brain abnormalities occur in the MTL hippocampus Memory De cits Earliest characteristic of AD is memory loss 0 The hippocampus is one of the earliest area affected and is most severely affected Can predict memory de cits of AD in order 0 In the beginning don t lose past memory but have trouble forming new ones eg getting lost easily anterograde amnesia 0 Then begin to have temporally graded retrograde amnesia P l nll l parietal E39 ilEEI Prell tantal mite 2quot39 milgtlala quot Enierhi39nal a r x A Inleriszar temporal Hi pntamriua tara Cellular Basis of Learning There are neuroplastic mechanisms at the cellular level these are instructors that are thought to be fundamental to learning and memory Hippocampus is very malleable at the cellular level For decades neuroscientists were looking for the physical change resulting from learning 0 Hypothesis was that learning involved a physical change at the cellular level 0 Went to a simple organism with a simple nervous system to study learning and memory Studying Learning in In vertebrates Eric Kandel one of the most famous neuroscientists today 0 Studied learning and memory in the sea slug Aplysia o Realized that other animals were too complex to study learning and memory Gill Withdrawal Reflex in Sea Slug ApgSfa Learning is necessary for survival in all species 0 Found that gill withdrawal re ex would change with expenence Gill withdrawal re ex in sea slug Aplysia 0 When in danger aplysia retracts its gill which is then covered by the mantle shelf o If you poke an area called the siphon it will withdraw its gill Have sensors to measure the tension when it is withdrawing its gill Habituation in the Aplysia o A decreased response to stimuli following repetition of stimuli 0 After poking the siphon several times the re ex is signi cantly lessened as measured by less tension o It realizes that its not in danger Sensitization in the Aplysia 0 An increased response to stimuli following some previous noxious stimulus 0 Shock its tail after touching the siphon noxious stimulus 0 After several trials the re ex is signi cantly increased Found that there is a change in neurotransmitter release as a result of learning 0 Habituation decrease in NT release 0 Sensitization increase in NT release LongTerm Potentiation LTP De nition 0 A burst of intense stimulation leaves a synapse potentiated or more responsive to new input of the same type for minutes days or weeks 0 LTP only happens in labs not in real life the type of stimulation used is larger than anything that could occur in nature arti cially induced 0 Thought to be similar to what occurs when we learn something Cells in HC are very amenable to LTP Hippocampus o Axon comes into HC and synapses on a cell body 0 This is the connection that LTP attempts to change Longterm change in the communication between the incoming axon and the dendrites and cell body in the HC Emraaa luar 39 mutiizulaLirit 7 39 namr ira quotee 39 r r 39 mutuality A r alactrmiaritna 7 r quot 39 alactmdan lhaa manila nail 39 39 layer w v39 1 39 FEEL a pulsar nr alimaariian a pulaa al aiii ulajlan iaaa ammiaia39ra 1 ag pa arani pain amlniaiaia 1 ag l l r aria again aria Ina haaa aa ramcame was 1 Iaiai in aaaaaa Ina racai a an aal raaailulai magail uaa Ell aha firml a1 iha in tha granule all Iargrar Famanliailan Hanna mama a39l Thaa maisa39ral I39raiaa a1 mama High LTP is ma mraaam aimiiuaa a1 Ii39EI iJElFl 39y ali ulalim mara applia quotilflE p pui l in ma aaaag 1 1h pearlmanl Z1Fi39i Ia inrdirjaa Ih39a lha apilm maata tha Firing al39 a LiTF39 graaiar minlanai a granule cilia i Futiula ljun EDTEE Elimulalitln 1 ma after 1 wank a m Eaanlllnia In Lmlan lrudu lari Stimulating electrode is at the incoming axon connecting to the cell body in HC Recording electrode is in the extracellular space in the HC 0 This is why the graph looks negative the extracellular space becomes more negative as the inside of the cell becomes more positive during AP Method a Administer a baseline stimulation i Represents a normal response in absence of LTP b Administer a highfrequency stimulation HFS c Wait one day after HFS d Administer the baseline stimulation e One day after HFS baseline stimulation produces a much larger response i This is longterm potentiation change in the synapse occurring after HFS f One week after HFS baseline stimulation produces a normal response again i Going back to normal ii Can make it more longterm by repeating process for long period of time Why is there longterm change in the ef cacy of the synapse 0 Major neurotransmitter involved in HC communication is glutamate o Glutamate is released at the synapse in the HC 0 Glutamate binds to both types of glutamate receptors AMPA receptor ionotropic When glutamate binds sodium enters the cell 0 Sodium depolarizes the dendrite and makes the cell excited makes it more likely for an AP to occur NMDA receptor ionotropic There is a magnesium molecule blocking the ion channel so even when glutamate binds nothing can enter the cell 0 When HFS occurs A lot of glutamate is binding to the receptors AMPA receptors allows a lot of sodium to go in which signi cantly depolarizes the cell This depolarization causes the magnesium block to lift magnesium molecule repelled from receptor site NMDA receptor allows both sodium and calcium to enter 0 When calcium enters it does good things and makes longterm changes in the postsynaptic cell 0 Thus calcium is necessary for LTP Calcium initiates processes to build more connections 0 A potentiated response a higher response due to more connchons Maintenance of LTP 0 Longterm changes like more connections that allow for an increased response LTP and memory 0 This is a very attractive model for what occurs when we learn How to see whether LTP is the mechanism for memory 0 Block NMDA receptors in rats during learning to see whether learning occurs or not 0 If LTP is the learning mechanism rats shouldn t be able to learn For the most part this has been found in research 0 Ex put a rat in a radial arm maze and allow it to learn where food is gt administer a NMDA receptor block gt rat won t remember where food is the next day Genetically engineered mice to have extra NMDA receptors 0 Hypothesis mice will be smarter 0 Results mice learned better LTP was more easily induced Hormones and Reproductive Behaviour Hormones De nition Chemical messengers that are released by endocrine glands into the bloodstream that act on target tissue or cells Any tissue that has a receptor for a hormone will be affected by hormone release 0 Receptors are speci c to particular hormones Similarities between hormones and neurotransmitters 0 Both are chemical messengers 0 Both act on speci c receptors Differences between hormones and neurotransmitters o Hormones have more widespread effects due to longer distance travelled o Hormones last longer Steroid Hormones A major class of hormones that are all derived from cholesterol Sex hormones are produced by the gonads ovaries and testes Action 0 Steroid hormones are fatsoluble so they can pass through cell membranes 0 Steroids go through the cell membrane gt enter the cell gt bind to nuclear intracellular receptors on the inside of the cell gt they then affect transcription 0 By affecting transcription they can make proteins Gonadal hormones primary sources are ovaries and testes 0 These hormones are present in all sexes what makes it different between males and females are the number of hormones circulating o Androgens Primary androgen testosterone o Estrogens Primary estrogens estradiol No such thing as estrogen class of hormones is estrogens o Progestins Primary progestin progesterone Sexlimited genes 0 Genes activated by sex hormones o Called quotsexlimited because effects are stronger in one sex over the other 0 Facial hair breast development etc are activated by sex limited genes quotP Control of the Anterior and Posterior Pituitary by the Hypothalmrus 7 7 Paraventrioulor 39 nucleus Postenlor Anterior I pituitary pituitary r Anterior Massa intermedia 4r commissure r connects the two 139 b n if 7 lobes of the thalamus VIP A Hypgrthalamiu39e I F Optic chiasm Anterior pituitary Posterior Mammillery pituitary body Farmrimular mime or wonmug Role of the Pituitary Gland and Hypothaamus O O BRAIN neiurai signals ANTERIOR PITUITARY releases gonadotropin 39 HYPOTHALAMUS releases genadolropin releasing hormone Anterior pituitary HT receives a signal that it either needs to increase or decrease release of hormones from the brain Neurons in HT release inhibiting and releasing hormones depending on signal received gt released into hypothalamopituitary portal system blood stream HT releases a gonadotropin releasing hormone GRH into the hypothalamopituitary portal system GRH tells the anterior pituitary to release gonadotropins into general circulation LH and FSH lutenizing hormone and follicle stimulating hormone Any areas with these receptors will be activated by gonadotropins Ovaries and testes have many receptors that pick up the gonadotropins Estrogens androgens or progestins are released into the circulation Other tissues are activated by these hormones Behavior is influenced by gonadal hormones acting on the brain HYPOTHALAMIC POFITAL SYSTEM Positive or negative feedback influences the subsequent release of hormones GENERAL CIRCULAWOiN BODY TISSUES Organizational Effects of Gonadal Hormones What are Organizational Effects Longlasting mostly permanent effects Effects persist when hormone is no longer in circulation In rodents sex differentiation occurs in the rst 3 to 4 months of prenatal development 0 Also extends into rst few days of life Helps researchers manipulate hormone levels to change brains Sex differentiation is harder to tell in humans but probably occurs later than 34 months Three things need to develop as male or female in this order 0 Primordial gonads testes or ovaries 0 Internal genitalia fallopian tubes etc females vas deferens etc males Miillerian ducts precursor to female internal reproductive organs Wolf an ducts precursor to male internal reproductive organs 0 External genitalia vagina or penis At 6 weeks all human fetuses are undifferentiated 0 Have both Miillerian and Wolf an duct precursors Male Development Genetic male is XY Y chromosome triggers synthesis of HY antigen testes determining factor TDF o SRY gene speci cally triggers synthesis of HY antigen 0 No Y chromosome no TDF HY antigen HY antigen acts on primordial gonads to trigger development of testes Testes release androgens testosterone and MUllerianinhibiting hormone MIH o Androgens cause Wolf an system to develop 0 MIH acts on Miillerian system to cause it to degenerate Result is development of internal and external male reproductive organs 0 In the presence of androgens one develops externally as a male At 6 weeks after conception the primordial gonads of XX and XY individuals are identical Medulla of the primordial Female XX If no Y chromosome is present the cortex of the primordial gonad o 04 matte gonad Male XY Under the influence of the Y chromosome the medulla of the primordial develops into an ovary gonad develops into a testis Female Development Genetic female is XX No Y so no synthesis of HY antigen No HY antigen so no testes ovaries develop No testes so no androgens and no MIH o No androgens so Wolffian ducts don t develop 0 No MIH so Miillerian system develops Females don t release any analogue to MIH 0 Thus Wolffian ducts don t develop because they need testosterone 0 But the Wolffian ducts don t generate because there is no hormone to do so 0 All females have remnants of Wolffian ducts in their systems but males have no remains of Miillerian ducts in theirs Result is development of internal and external female reproductive organs 0 In the absence of androgens one develops externally as a female Female is the quotdefault genderquot Testosterone is the precursor to estradiol the main estrogen produced 0 Aromatase is necessary to make estradiol Testosterone is also the precursor to DHT o 5alpha reductase is necessary to make DHT Hormonal Abnormalities in Sexual Development Congenital adrenal hyperplasia 0 When the adrenal gland secretes large amounts of androgens This usually occurs a little bit after development of Wolf an and Miillerian ducts so it doesn t affect internal genitalia past the sensitive period 0 Genetic females will have female gonads female internal genitalia but male external genitalia This all depends upon the timing and amount of release Some look completely like genetic males others look sexually ambiguous Sis anmpllm mm W IEIi rIHIE F Urathralfla 39 lLaiHrailbstaml quot rum MEI Earliaiin with H lm 39l39 quot x i 39 QM rr ii iii i l l Fully lMl39lbpalrd r ll f Eii ralmm Head ri l i llm in Fm EWING fig A f ifrll abiaiminma l iquot if i EI39LE39FE l HIEW l l Lquot l n n a y Emmuml L 1 l HILEElEzm jEHTE quota 391 s j V r 7 AKquot LA urm ifs Can have masculinization of the body and brain 0 When this happens in genetic males it doesn t affect too much Androgen insensitivity syndrome 0 Primarily impacts genetic males 0 Bodies and brains are insensitive to androgen Usually a result of androgen receptors not working properly Thus androgens can t have an effect 0 They have testes that release androgens and MIH Wolf an ducts don t develop because androgens aren t having an effect Miillerian ducts don t develop since MIH is released 0 They have no internal genitalia o Testes don t descend they remain internal This is because androgens normally act on testes to descend o Androgens are necessary for external male genitalia Thus female external genitalia is developed 0 Born looking like females but are genetic males Usually don t notice this until puberty when they don t get periods Genetic males normally have some estrogens circulating but androgens are circulating much more and so they have the predominant effect 0 In people with androgen insensitivity the little estrogens have a large effect because there are no other hormones circulating develop hips breasts etc 0 Don t develop any body hair because they don t have any androgens Two twins one of which had an accident with his penis when he was younger so the doctor just cut it off and the parents raised him as a girl 0 He never felt adjusted eventually was told the truth and began to live as a male 0 Eventually committed suicide 5alpha reductase de ciency 0 Don t have an enzyme called 5alpha reductase 0 During prenatal development testes release androgens especially testosterone Testosterone can be converted into other hormones Dihydrotestosterone DHT T gt DHT as long as 5 alpha reductase is present the enzyme that helps convert it 0 Have normal testosterone circulating Wolffian ducts develop normally Miillerian ducts also inhibited 0 External organ development is due to DHT not testosterone Thus people with this de ciency don t develop male external genitalia they develop female external gentaHa 0 Look like genetic females when born But they have male gonads internal testes and internal genitalia Sexual Dimorphism of the Mammalian Brain Sexual dimorphic structure a structure that is different across males and females There is sexual dimorphism in the brain at all levels 0 Cells synapses neurotransmitters structures connections etc Sex differences in the human brain 0 Men s brains tend to be 15 larger Attributed to difference in body size 0 Numerous differences in volumes of various nuclei and bre tracts number and type of synapses etc o Ongoing work as to the signi cance of these differences For years most research was done on males assumed that females were the same Need to know what can be affected by sex Rodent studies 0 Early studies and transplants of gonads Castrated a male rat on day 1 look female as adult 0 Can t do this with an adult rat 0 Absence of hormones organizes brain as female Removed a female rat s ovaries on day 1 had no effect as adults 0 Has no estrogen as an adult but still has gonadotropins being released as a female 0 Absence of hormones organized brain as female Transplanted testes in a female rat on day 1 looks male as adult 0 Presence of T in sensitive period is what makes the brain male Follows the same pattern as the body Transplanted ovaries in a male rat on day 1 Gonadotropin levels vary across menstrual cycles in females 0 Used to check which type of brain was made male or female when manipulating hormones in early development Thus hormones organize both bodies and brains during sensitive period of development 0 Found that Presence of androgens gt male brain Absence of androgens gt female brain 0 Sexually dimorphic nucleus SDN of the medial preoptic area MPA of the hypothalamus MPA is a bunch of nuclei located a little before the optic chiasm Larger in males small or nonexistent in females Ovaries don t play a large role in sexual differentiation 0 Testes are very active during pre and perinatal development Sexual Dimorphism of the Mammalian Brain Rodent studies 0 lnferred sex differences in the brain by measuring gonadotropins lf gonadotropins are cycling brain organized as female lf gonadotropins remain constant brain organized as male 0 Presence of androgens during the sensitive period male 0 Absence of androgens during the sensitive period female 0 Sexually dimorphic nucleus of the medial preoptic area Large in males almost nonexistent in females Gave female rats testosterone Increased the size of their SDN to match a males Castrated male rats Decreased the size of their SDN to match a females Castration has to occur during the sensitive period rst few days of life Hypothalamus and sexual behaviour 0 Males medial preoptic area via projections to lateral tegmental eld Destroying this area takes away sexual behaviour of males mounting 0 Females ventromedial nucleus VMN of the hypothalamus via projections to periaqueductal grey Important for lordosis destroying area will take away lordosis Large in females and small in males 0 Can be reversed through injecting opposite hormones during sensitive period Reorganization of reproductive behaviour 0 Castrating male rats or injecting T into female rats during the sensitive period will reverse sexual behaviour Make males exhibit lordosis and females mount corpus 1W5 callosum Lateral ventricle 35339quot I Halaliuo ll39nilunmul39 the Emutally Elmammo HWDEEII IJTI lllu l t Flam Supraohiasmalio Optic Sexually nucleus 7 chiasm dimorphic nucleus iEiUEE 3 EE g TEEEa E E idea E3 32 35 25 7 gun aairaiim calmalien Hormel on may 1 am ag a Ma a Guamoi Fatiguedle gitElly c I I ml 139quot r a 39 1i H39sv 2 a H a H as Ina r a ll v Lateral lli aizllal K W v preeplin r r WEIIE MGChanism39 mm Umtrlmmmi H mm BUB EFE 3 WWW Many different ways to tell masculinization different brain areas behaviours etc i llnlla 33ml eireuili Rodent studies 0 Role of testosterone Presence of testosterone male brain Absence of testosterone female brain 0 Aromatization to estradiol responsible for masculinization of the brain Testosterone travels through the blood and reaches the brain There is a lot of aromatase in the brain This aromatase converts testosterone to estradiol Estradiol acting on receptors during sensitive period allows brain to develop as male 0 This is why ovaries don t release estrogen during pre or perinatal development otherwise genetic females brains would develop as male Injecting hormones only works during sensitive pedod Nuances o Injecting T to female male brain 0 Injecting T aromatase inhibitor to female female brain Injecting T to castrated male male brain Injecting E to castrated male male brain Injecting DHT to castrated male female brain 0 DHT can t be turned into E o Injecting aromatase inhibitor to normal male female brain 0 Alpha fetoprotein Humans This circulates in high levels during early development This binds to estrogen circulating from mother s ovariesblood and stops it from crossing the blood brain barrier 0 Thus very little estrogen from mother gets to the brain This is true for both males and females AFP doesn t bind to testosterone so T crosses the bloodbrain barrier and is then converted to estradiol which allows for masculinization of the brain 0 This is what protects females from being masculinized When injecting estrogen there s not enough AFP to bind to all the estrogen so injecting estrogen still masculinizes the brain 0 Aromatization not necessary Either testosterone or estradiol can masculinize the brain Human brains also have high levels of aromatase o T will be converted to E which can masculinize the brain Genetic males who have aromatase de ciencies still develop a male brain thus androgens can directly masculinize as well 0 Estradiol is capable of masculinizing Thus something still has to protect females from having a masculinized brain Placental barrier o AFP is not as important in humans as it is in rodents Placental barrier keeps mother s estrogen from reaching the baby s brain 0 However if we give arti cially high levels of estrogen through injection the placental barrier is not enough to protect it and the brain will be masculinized Synthetic estrogen DES 0 Given to mothers with a high risk of miscarriage The female offspring of these mothers had slightly masculinized brains 0 Higher incidence of homosexuality than others 0 Other mechanisms There are some sex differences in the brain that occur prenatally before the hormones are released Suggests that hormones are not the only mechanism for sexual differentiation of the brain Sex chromosomes may contribute having a Y chromosome Helaulva 39munw 4 Eh Egalith l lm pl ll Hum lim uizlluill REES Holalll39a39n39ii39mlunw nl39 Eh gunman llmdmphla Eltli BIEEll In i u tl lt Flam 5503 155qu Famala alas Elanaim lli39l t39li l l on a 775 51 EUEE39EE 25 Tiasteam runa Ih j t39 i l m1 E1514 4 all mm laeiraiim Emtralion Hanna run any 1 my Em a1 mu Emutil E Tna Lilli 25 Activational Effects of Gonadal Hormones What are Activational Effects Effects of hormones in the adult brain Usually temporary and persist only when hormone is present Act on the circuitry that has already been organized as male or female Sexual Behaviour in Rodents Due to activational effects acting on organizational circuitry Injecting female rats with testosterone when young will only cause male sexual behaviour mounting if one injects them with testosterone when older as well If one castrates a normally developed male rat it will not mount however if one injects testosterone they will exhibit normal male sexual behaviour mounting Experiment on male rats 0 Grouped into ow medium and highdrive groups 0 Castrated them all to wipe out sex behaviour 0 Gave all the same dose of testosterone o All went back to their original sex drive low medium or high despite being injected with the same amount of testosterone Adult rats need sex hormones to engage in sexual behaviour Sexual Behaviour in Humans Castrating an adult male arti cially or naturally will reduce sex drive Postmenopausal women sti engage in sexual behaviour despite lack of hormones Attempting to see whether there s a change in sex drive across hormone levels usually experiment on women on birth control vs naturally cycling women 0 Usually engage in sex more when hormone levels T are higher 0 Women on birth control don t have as many variations in hormones as naturally cycling women do m ulai r i a liiriiiif Reward Circuitry and Addiction Rewarding Behaviour Adaptive mechanism exists whereby Example 0 A wild mouse is hungry and is motivated to nd food 0 Finding food must be rewarding so that the mouse will do it again process by which it obtains food has to be remembered so this process has to be rewarded as well Natural rewards are good and adaptive 0 We have a brain mechanism by which we will repeat these behaviours MotivationReward Circuit Meso midbrain telencephalon thalamus and forebrain Dopamine is very important for reward circuitry Several sources of dopamine o gt widespread areas of cortex etc o Substantia nigra gt basal ganglia striatum Nucleus Accumbens Particularly important structure for reward Arti cially injecting dopamine to the NA is very powerful o Rats would rather bar press for this injection than for food Almost all drugs of abuse will directly or indirectly increase dopamine release in the NA Amygdaa PFC Important for 0 When something is very rewarding PFC helps control use of this Striatum speci cally habits of using drugs FIGURE 158 The mesotelencephalic dopamine system in the human brain consisting of the nigrostriatal pathway green and the mesocorticolimbic pathway red Based on Klivington 1992 VP Striatum Most things that go to the cortex stop off at the thalamus along the way Hippocampus helps make memories Jr Il Limblc 1 quot39 cortex Dorsal striatum r E A l v Prefrontal y Ventral g iquot39 area J Nucleus K K accumbens ffgig Olfactory tubercle Amygdala Septum Substantia nigra This is the Striatu Hthg39lt I4 I Si111li39 Lina3111 t j a ll lliZL5Jii i tnrl E HHt L39E i TH irra39t wufl in TU39 dl t l am l drug chil39lazthg 11 12hr nmm39i circuit PHquot prurl rcinial L39tif l39 MU Iilff39li iW il flii liilil39hi HP lil39l PLi39quot castlpug 15153 L39I tn nlntuirnl fling gaialdg 39II I I39I lcg lriiml arisen nucleui acrunibcm Functional Implication of Circuitrv Reward circuitry provide a pathway by which the structures that are involved in reward emotions decisionmaking memory impulse control and habit are NA is the centre of the circuitry Coordinated in an adaptive way helps us survive Coordinated in a negative way allows it to be hijacked by drugs Comparison of adaptive reward learning and development of addiction Biological Re ward System Initial exposure to biological reward causes increase in DA levels in NAc Convergence of DA and glutamate at synapses in the NAc crucial for integration of information Repeated exposure to biological reward results in progressively decreased release of DA Thus predicted rewards do NOT increase DA So under normal circumstances DA is signalling the reward circuitry to learn associations that predict a rewarding stimulus Drugs of Abuse An initial exposure to a drug takes advantage of the same circuitry as a biological reward Like natural rewards addictive drugs encode and reinforce drug seeking behaviour by regulating DA and glutamate release in NAc But each exposure to drug results in DA release as if it were the rst experience with a reward So unlike natural activation of reward system which adapts to repeated exposure pharmacological activation of reward system causes repeated and maintained release of DA This continued release continuously engenders new associations and may cause the learning associated with drugs of abuse to become pathological quotSuper consolidationquot results for 0 Memories for the motivational stimuli o Behavioural patterns used to satisfy the desire o Stimuli associated with the drugs The consolidation is glutamate at the same time as dopamine which only happens the rst few times for natural rewards Addiction makes it to where this glutamate and dopamine consolidation happens over and over and over and everyime making it a superconsolidation Results in lordterm dysfunction of PFC NAc communication Summary Learning about natural rewards and learning about drugs of abuse involve the same pathways in the brain Repeated use of drugs results in changes in the brain that are not associated with repeated natural rewards 0 They think its because of this continuous release of dopamine that doesn t happen with natural rewards Repeated pharmacological activation of reward system alters the functioning of many structure but important for addiction the NAc and PFC 0 We think the connections between these become ultra long term physical changes in the way they communicate with each other The pathology of drug addiction appears to arise from the repeated use of a drug that induces a kind of superconsolidation of the memories for the drug 0 Because of this continuous release of dopamine there is a superconsolidation that we think becomes a physical change Some people are more susceptible to this change But Eventually based on animal models give enough time and drug they can all get addicted Treatments based on counteracting some of the longterm dysfunctional changes are being investigated 0 What if we try to manipulate the connection to the PFC and NAc maybe block the receptors Behavioural paradigms animal models of drug abuse research Selfadministration provides information about the addictive properties of a drug o If you have them administer it themselves it becomes more addicting than if they didn t give it to themselves they have to work for it 0 Depending on how addictive the drug is They re going to work harder for the more addictive drugs press the level more ie they press the level so hard and often that they almost kill themselves trying to do the work for cocaine Conditioned placeprefrence provides information about the rewarding properties of a drug 0 Rats given a choice want to go to the dark side 0 Give them a shot of cocaine and then force them to go to the light side 0 The next day give them saline and make them stay in the dark If you do this enough and put them in the box to chose they ll hang out almost the entire time on the light side because they ll associate this place with cocaine 0 This is how they test if a drug is pleasurable and can tell if its addictive 0 There s a doctor downtown who is making a drug as powerful as morphine but doesn t have the addictive properties Could do this test with morphine in 2 weeks and they ll hang out on the light side after The same testing with their new drug results in rats not having a preference shows the drug is not addictive or pleasurable Lecture 041615 Sleep Endogenous Circadian Rhythms Endogenous coming from within Circadian daily Rhythms that last about a day Ex if one is staying up late will be more tired around the time they re supposed to go to sleep than they will in the morning Biological Clock Internal mechanisms that maintain the circadian rhythm FreeRunning Rhythm Rhythm that occurs when environmental cues are absent Original experiments say that freerunning rhythm is 25 hours or longer 0 May be biased because people in experiments leave a bright light on until they re ready to go to bed may prolong the rhythm 0 May be 242 hours not as long as original experiments show This extra 02 hours could accumulate over days to make someone completely out of sync with the rest of the world h Things they tell you not to do before you go to sleep are all Zeitgebers 0 Eating a lot high activity etc jet Lag and Late Shifts Jet lag when internal clock and external world are out of sync Late shifts 0 Working all night and sleeping all day 0 Not good for the body Biological Mechanisms of Circadian Rhythms Difficult to get rid of circadian rhythms o Experimentally blind animals still have rhythms get out of sync a little but they still maintain them Located right above supra the optic chiasm in the hypothalamus Lesioning the SCN gets rid of circadian rhythms Famous experiment O Mutant hamsters with 20 hour rhythms Suspected the SCN was responsible for this 0 Took the mutant hamsters SCN and implanted it into normal hamsters and viceversa O 15 Transmittaln not In eliminate lhE almlily I n lia tii39ftlark cwlwu 39Ii39u Eh ll ii l Laiuadia rl39rwhms l f Trananat tin 5 F K H EliminateIr 1h 5 n i z m l A abil y of Hitdart a A cycle31 em iam r 39 Elma iers rtr trnau 39l r 391 JP r r Pia 7 393 axt r J 39 quot2 a I Emmott l in 39 IH39quot n c whimn ii nal quot quot n F quotI pf H39ud39 JUPTJEJ39EIESMIII 15hquot JA H uclam quot l NH Him 7 unkquot Iii herm i l A i F r n u U H J Retmorrrpamalarrii H a r lrnzi u E i x in II xv This Euggsmdn 39at quot1E a quot aanseqlmats marl madia la Ihn Enirzainmmril k a 431 Camden rhythms tr li t darh cycle tranche171nm the np li chiasm and Newest to the ambas rnati nuclm 31 E39m Ilrgpmiulamus F 0 During the day production of these proteins is increased 0 During nighttime production is decreased 0 Experiment on RHT in blind animals Lesioned the optic nerve right before the optic chiasm This messed up circadian rhythms Lesioned the optic nerve right after the optic chiasm o This did not eliminate circadian rhythms Transatlsion mt r Elil39r lil 39lEll lis l ailquotji r limitdark mailm v Transat tin H Elil i ill l 1h 5 i i Ei l ii l Laiizadla trimmera abil y a lightdart 39 l 1 eniialn Ell39lf l ilil39i minima ga 1 r r 1 iii Fquot39 E j 39 9 an L cm was quot H Elplir schiam A HTnil i I 99 r Suprathiasmlil 1 r Madame 77 nucleus I PF In a l r I 39 AMJ 39 lplll herm L P 1 Ftatmzl39rrLathal mm Imizi u E l 13 i5 I r l L g L w This Euggs znrd ij39at H15 an u 77 II quot ab 7 D quotquot assiaan mtHi1er at medium llm Enlrzair imril k a m rhythms tr light dark P uynles branch ll39lnzurn the Elip iii39 chlaam and pmest to the embass rnati muchn nquotl Em tglp li39alamus Regulates levels of melatonin behind the thalamus Melatonin levels increase before a person gets sleepy o Mechanism by which it regulates sleep is unknown Scientists think melatonin helps you get sleepy 0 People used to think melatonin pills would help Doesn t help sleeping very much But it does help jet lag slightly Other Mechanisms There is still evidence of rhythms in people whose SCN is lesioned Every cell in our body has some type of biological clock Stages of Sleep Can assess stages of sleep through EEGs Until this was available there was no objective way to tell if someone was asleep 0 With EEG researchers objectively know if people are asleep or not Alert wakefulness duet befeire eleep Alpha waves Stage 11 Sleep spindle K complex Stage 3 Siege 4 lllllilllllllll Stages of Sleep During wakefulness o Amplitudes are low no consistency across the brain since some parts of the area are very active while others aren t o A lot of activity thus frequencies are high During seep 0 Very little activity frequencies are low 0 Whole brain is active during sleep amplitudes are high 0 Frequency 812 Hz cycles per second F 0 When someone rst falls asleep ie eyes rolling in the back of your head o Respiration and heart rate begins to slow 0 These two patterns especially sleep spindles may be the mechanism to especially those who have trouble going to sleep including recovering alcoholics 0 slow waves 12 Hz 0 Sensory input to the cortex is signi cantly reduced 0 If less than 50 Delta waves Stage 3 o If more than 50 Delta waves Stage 4 0 Used to be called quotparadoxical sleepquot Paradox body doesn t move but mind is very active 0 REM also called Emergent Stage 1 looks similar to Stage 1 Sequence of Sleep Stages Most deep sleep occurs in the rst half of the night Most REM sleep occurs in the second half of the night I EEG Stages During a Typical Night s Sleep Periede of REM Lack of coremuscle tone Awake 5 Stage 1 g c e Stage 2 ILL Stage All 1 2 3 4 5 B 8 9 H 39Lllllf39E Sleep Disorders Many causes of insomnia drugs medicine stress excessive noise too much light exercising too close to nighttime unknown causes Many types of insomnia o This wakes the sufferer up Don t get a good night s sleep because of this 0 Sudden attack of extreme sleepiness o Often happens when one is particularly alert 0 Can happen in people without narcolepsy 0 When one is beginning to wake up awake but can t move In the middle of REM sleep and wake up 0 Can happen in people without narcolepsy Difficult to test scienti cally 0 Some scientists believe this is untrue say one is partially awake Very rare usually a result of brain damage usually to the pons Most people have muscle paralysis during REM 0 People with this disorder don t have muscle paralysis Act out their dreams during REM sleep Night Terrors Sleep Walking Do not occur during REM sleep 0 Mostly occur during Stages 3 and 4 Can dream during other stages of sleep not as frequent or vivid as in REM Night terrors usually occur in children 0 Wake up in the middle of the night and start screaming 0 Usually can t tell you why they re so scared Fatal Familial Insomnia Genetic disorder extremely rare a prion disease Usually onsets in middle age Can t sleep at all causes death Giving sleeping pills doesn t work go into quottwilight sleepquot never actually sleep Biological Mechanisms of Sleep Arousal Reticular formation pontomesencephalon o Spans the pons and mesencephalon 0 Active during wakefulness o If destroyed one will go into a period of prolonged sleep from which they are unable to be awoken 0 Will not be asked about NTs relating to this structure Only asked about those that are written on the slides Locus coeruleus in the pons 0 Totally inactive during sleep active during wakefulness especially during meaningful events or when paying attention to something 0 May aid in memory especially for meaningful events 0 May be a reason why we don t remember our dreams Basal forebrain GABA ACh adenosine o A source of acetylcholine excitatory and GABA inhibitory Released all over the cortex When ACh in control one is awake when GABA in control one is sleepy 0 Presence of adenosine Not actually a neurotransmitter it s a metabolic product Function inhibits acetylcholine activation in the basal forebrain So that one will get sleepy and GABA can take over Adenosine levels increase while one is active during the day Monoadenosine broken down into adenosine as a result of activity A lot of adenosine is built up in the basal forebrain In the morning low adenosine levels high ACh awake At nighttime high adenosine levels low ACh geepy o Caffeine blocks adenosine receptors This stops inhibition of acetylcholine disinhibition Thus ACh continues to be released and one will stay more alert Hypothalamus histamine 0 HT contains both inhibitory and excitatory neurotransmitters Histamine is excitatory 0 Release of histamine keeps you awake Interacts with the basal forebrain don t worry about this 0 Histamine is also involved in allergic reactions Take antihistamines for allergies but this medicine also makes you drowsy blocks histamine s ability to keep you awake Signals that Indicate Sleep Decreased body temperature 0 Signal to the brain to shut down excitatory system and increase sleep system Decreased stimulation 0 This is why you shouldn t exercise at night use the computer or watch too much TV at nighttime Decreased arousal REM Activity in pons o Burst of activity when rst entering REM Signal to spinal cord 0 Pons sends a signal to the spinal cord to shut down muscle activity Ponsgeniculateoccipital PGO waves 0 Pons then sends information to the thalamus particularly the lateral geniculate nucleus LGN 0 Then goes from the thalamus to the occipital lobe o Pons gt LGN gt occipital lobe 0 These waves are unique to REM sleep Not sure exactly why but only seen here Brain mechanisms of sleeping and waking Green arrows indicate excitatory connections red arrows indicate inhibitory connections Neurotransmitters are indicated when they are known Although adenosine is shown as a small arrow it is a metabolic product that builds up in the area not something released by axons During REM F Wires FansGenilculieElttlpl i lj J 312 r L J quot 1 g 3 L 11 4 r 393 r a i i A 5D mi r u 1 ifquot in 39 39 33 3 1 AF a a wit 7 m 7 T E 1 quota 1 u 1397 r H u39 7 1 GEE31E nilme r Nucleus quot pm chnc lp39lll Earle 1 Signal from pons to spinal cord Sends message to suspend muscle activity Purpose of Sleep Circadian Theories of Sleep Sleep is not a reaction to the disruptive effects of being awake The internal clock evolved sleep to keep us away from danger at night 0 Before electricity walking around at night was dangerous eaten by predators can t see etc 0 Sleeping is safer than being awake Not many people still believe this 0 Still some support this may be why we re not nocturnal Recuperation Theories of Sleep An animal that doesn t sleep will die 0 Eat more than normal but they waste away 0 Immune system shuts down body and brain doesn t work properly 0 This observation was the original impetus behind the recuperation theory We sleep to allow our bodies and brains to recover from the demands of being awake 0 Originally just a hypothesis now have some evidence Research 0 Looked at the brains of mice O Developed a tracer to see microscopic levels of CSF 0 Found tiny uid lled channels that go throughout the brain More CSF when the mouse is asleep rather than awake 0 Thought that these channels allow an exchange and clear toxins 0 Gave the mice anesthesia in the middle of their wake cycle still see the same pattern of increased CSF channels 0 Sleep improves clearance of waste in the brain ex amyloid betas Thus if one doesn t sleep clearance of waste will not happen as rapidly as it normally would and one will die from accumulation o This data was the first to support the recuperation theory of sleep From PowerPoint 0 Sleep may increase the brain s ability to quotcleanquot itself 0 Sleep associated with increase in network of CSF lled channels that clears toxins from the brain 0 Related to sleep and not circadian rhythms because anesthesiainduced sleep results in similar patterns as natural sleep Proves that circadian theories don t explain why we sleep Evolutionary Considerations Looking across species for commonalities All mammals and birds sleep even if they re at a greater risk of predation during sleep 0 Sleep itself must serve some function and not just a way to escape All mammals and birds sleep 0 Sleep is not a higherorder human function Large betweenspecies differences in sleep time 0 Sleep is needed but not always in large quantities No clear relationship between species sleep time and level of activity body size or body temperature Why Do We Have REM REM Deprivation If you deprive someone of REM sleep they will make it up on subsequent nights Sleep study 0 Every time they see someone going into REM sleep they wake you up Will be woken up more and more over time 0 Thus subjects are not deprived of deep sleep but just REM sleep 0 Without REM subject will cycle into REM quicker when they fall asleep and spend more of their night in REM sleep than normal Predeprivation 20 REM sleep Postdeprivation 30 REM sleep 0 Called quotREM Reboundquot attempting to make up REM sleep Memory Storage Sleep particularly REM may play a part in memory consolidation 0 Moving STM to LTM Plasticity occurs as a result of sleep Watching a rat s brain at night after they ve learned something new during the day shows higher brain activity than normal lnverted owerpot method 0 Fill it with water and put the rat inside on the raised surface 0 Can do it one of two ways Deprive them of all sleep every time the rat falls asleep they ll fall off the surface Deprive them of REM sleep have a bigger surface every time the rat falls into REM sleep they ll fall off 0 Yoked control Don t know whether the rat didn t learn because they re stressed out from being woken up all the time or because they didn t sleep Yoked control group have another group of rats fall into the water a similar number of times as the sleep group but don t make them fall while they re sleeping Thus these rats will be just as stressed out as the other rats but the component of sleep will be absent Why Do We Dream Freud etc Discredited His theories of dream interpretation have been proven false May have been slightly correct 0 One can dream about events that have happened recently or that are stressing them out Activa tionSynthesis Hypothesis Especially during REM one s brain is active but is receiving no sensory input from the outside world Since memory consolidation is occurring random memories are being activated o Prefrontal cortex likes the world to make sense so it has to do something with this Prefrontal cortex attempts to make sense of the random activation of scattered memories so it makes them into a story 0 Thus things that are on one s mind will show up in one s dreams but will not necessarily make sense FEElilh lwp mErnlui 39il gn n h r will Tinni Sublimh a View to Enlam E El 51 5 E F Him 01 awlw m Imrrnbm39 If mhanng to 1 miljniz null HEM Heep i mi i a as lite lierind all deathalien ensues Prid isrmalma F l prluglr m quot l a i H I m u i u mr r gt v74 i n l n V FIMH L39EI Total ELIFIF Tl39lrm Emntln HEM snap M a Cl 55 aquot 12345533935139D ll1 i1213 Him h nrarpign dl qi39FlEM j fl Iglg 39iugm n 511W 1 War PIEH LEELIE IZI39I II IEli EWIEiFI HEM EILEEF
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'