Brain and Behavior (Biopsychology) part 1
Brain and Behavior (Biopsychology) part 1 103
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This 31 page Study Guide was uploaded by Amanda Huang on Friday October 9, 2015. The Study Guide belongs to 103 at Tufts University taught by in Fall 2014. Since its upload, it has received 60 views. For similar materials see Brain and Behavior in Psychlogy at Tufts University.
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Date Created: 10/09/15
x 39 5 39 U I aquot x 39 quots l w x r Terminal I fryn buttons 4 97 41 r4 LECTURE 1 WHAT IS BIOPSYCHOLOGY Soma p I Biopsychology study of physiological genetic contributions to wequot Mye shea h behavior 7 Iquot l quot I I Strong emphasis on experimental design statistics 39 Axonanside 39 myelin sheath I CNS brain spinal cord vs PNS sensory organs and nerves Directionof v collectlon of neurons messages I What are the functions of the nervous system I 3 function of nervous system gt 1 Gather info sensory 2 Integrate info processing 3 Act motor response I these functions need cells specialized for communication and analysis NEURON neurons make up the nerve Role gt Dendrite gathers info all over dendritic tree from outside other neurons changed by experience I Messages from neuron to neuron are transmitted across the synapse gt Soma cell body integrates info action potential between soma and axon gt Axon respond and send the info on to the terminal buttons I Carries action potential brief electricalchemical event I Action potential is ALWAYS same size and duration gt Terminal Button When a action potential reaches TB neurotransmitter is secreted excites or inhibits receive cell I Action potentials only in the nonmyleinated sections node of ranvier of the axon I Standard image of neuron only exists in the spinal cord I Axons are only myleinated for messages that must travel long distances INTERNAL STRUCTURE of a cell I Nucleus enclosed by the nuclear membrane nucleolus produces ribosome and chromosomes I Noncoding RNA ncRNA makes up part of splicesome cuts splices mRNA I Cytoplasm gt Mitochondria double membrane that produces ATP gt Endoplasmic reticulum storage and channel for transporting chemicals through cytoplasm I RER has ribosomes embedded I Proteins produced by ribosomes are either transporter or used in the membrane I SER channels for segregation of molecules lipid molecules also produced gt Unattached ribosomes produces proteins used Within the neuron gt Golgi apparatus part of SER I Complex molecules assembled or packaging agent I Produces lysosomes small sacs that break down things no longer needed later recycled or secreted gt Cytoskeleton gives neuron its shape I Made up of 3 protein strands v To brain Te r m mal buttons IL Unipolar NEURONS CLASSIFICATION I of neuronal processes gt Unipolar one stalk that splits into 2 branches splits into directions one to peripheral other to central nervous system I Like bipolar neurons transmit sensory info from environ to CNS I Cell body right next to the spinal cord dorsal root ganglia gt Bipolar one axon one dendritic tree at opposite ends of the soma usually sensory I In our head related to the senses interneuron gt Multipolar somatic membrane gives rise to one axon but many dendrites most common I Function gt Sensory neurons toward brain AFFERENT gt Motor neuron9 to muscles EFFERENT think of as existing gt Interneurons CONNECT cells some don t have action potentials as the axons are so short ONLY in CNS I Local interneurons connect nearby neurons and analyze small pieces of info I Relay interneurons connect collection of local interneurons in one part with y A 1 p quot 7quot Emggm those in another region quot 39 Lame gel I Neurotrasmitter used by a neuron or responded to I Genetic markers what gene they express Golgi and Cajal I I Golgi developed 1st stain that reveals the external forms of neurons gt v I 512231 I Caj al used Golgi stain to expand study of brain circuitry X CNS SUPPORT CELLS I GLIA glue physical support control nutrient ow involved in phagocytosis gt Astrocytes provides physical support ll in space left by neurons that have died transport nutrients to neurons help regulate chemicals at the synapse I Can replicate don t have action potential I Brain blood barrier Screens things out of the CNS I in the body cells that line the capillaries are not tightly fit but in the CNS there is no gap which forms the BB barrier I Break down glucose from capillaries and break it down to lactate which is then released into the neurons I Glycogen is stored in small amount that can be used when the surrounding neurons have a high metabolic rate gt Oligodendrocytes Physical support and form myelin sheath around axons in the brain outside brain spinal cord done by Schwann cells I Forms lipid bilayer gt Microglia involved in phagocytosis cleaning up debris brain immune function I Can move around Biology is NOT only supportive of nurture but also largely nature I A lot is based on the experiences of the environment I Ex Genetic component to major Depressive Disorder gt Variation in gene for the serotonin reuptake protein is linked to depression but only as an increased vulnerability to stressful events gt Rats in enriched environment had thicker cerebral cortices higher concentration of AchE more complex dendrites Unipolar Bipolar Cells of the Central Nervous System Microglia LE CTURE 2 ELECTRIAL PROPERTIES OF NEURONS Nerve cells specialized for communication neurons conduct ELECTROCHEMICAL signals Neurons receive CHEMICAL messages from other neurons Chemical messengers activate receptors on dendriticsoma membrane Receptor activation alters ion distribution alters electrical charge and across the membrane Action potential can result then is propagated down the axonal membrane Action potential causes release of transmitter from axon terminals to communicate w neighboring cells In nervous systems CHEMICAL communication between and ELECTRICAL within VV VVV PROPERITES OF NEURONS AND COMMUNICATION Chemical Environment 2 critical factors in neuron s ability to communicate are 1 Chemical environ 2 Cell membrane boundary controls the environ gt cell membrane lipids and proteins 0 J go Outside of Cell Cannot leave InSIde of Cell Ge Force of diffusion chemical equilibrium distribute equally in concentration Higt Lo Force of electrostatic pressureequilibrium gt Electrostatic pressure the pull and push of charges Distribution of ions across the neuronal membrane 131 O Or Qua Ion Concentration in Concentration o I I I gt Net charge of charge 1ns1de neurons 70 mV approx 339 32222 433 528 mM quotIV I Neg charge result from the neg charge of proteins Na sodium 50 460 56 inside the cell A39 Proteins 345 1 gt Nerst eq calculates electric force necessary to balance a concentration a i r I When calculated the values don t show proper values for the inner voltage I Assumption that the ions were freely permeable but its NOT Sodium channel Cl d O R f t R t O 3 The cell membrane 1s selectively permeable Se pen awry 656 I pred1cts what force is necessary to balance the force of d1ffus10n Sodium ions enter High concentration concl ginration F Na 40 39 Na channels I become K Force of Electrostatic Force of Electrostatic refractory no difquIon pressure diffusmn pressure more Na enters cell 39 39 A 39 39 39 39 39 E K continues to E 0 Ileavecell g causes membrane 23 K Chanfels potential to return 0 Opel K to resting level ac begins to leave 9 cell I X GE Na channels Force of L Electrostatic g Na 2 open Na diffusion pressure begins to eme K cell K channels close I Na channels reset 70 v ACTION POTENTIAL can go BOTH anterograde amp retrograde Threlshold of I excitation I Steps gt 1 Vd Na channels open and Na goes in Why depolarization of the cell less neg before it reaches equilibrium of Na at 40mV vd Na channels close I Tetrodotoxin TTX shuts down vd Na channels prevents depolarization gt 2 K out AP decreases gt Tetraethylammonium TEA shuts down vd K channels prevents polarization gt 3 Na channels are fast but K channels are slow closing which cause hyperpolarization for a brief moment before the K channel closes relative refractory period Absolute refractory period voltage dependent Na channels are resetting I Neurons CAN NOT produce an action potential more quickly than lmillisecond gt Relative refractory periods hyperpolarization stage when K is still closing 3 sodium Ions quotW 16 i in L out Sodiumpotassium 32 I quot quot30830me Q Na quot3 Dub of Cdl i 39 Membrane Na 0 Falling phase 01 the action potential t i H 6 x quot Actlon potential quot 1 l vquot i 1 a a a eeggs ewmyigsm E lnsldoofColl w i Ko 2 potassium lons pumped In 39 t II I cwosol l 6 Sodium 39 Inactivation channel gate 0 Resting state I PROPERTIES gt All or none resting potential makes it pass the threshold or doesn t gt Fixed amplitude unless there is something extraordinary gt Absolute refractory period Where stimulation Will not produce AP gt depended on voltagedependent Na channels I typically only found on axonal membranes I Why doesn t it break down SODIUMPOTASSIUM PUMP transporter protein gt Uses ATP each time to help restore NaK balance gt ONLY axons have voltage activated Na channels gt What of a region of cells Wout voltagedependent Na channels How about a part of the cell Wout vd Na channels Decreased conduction of local AP I Graded local potentials local disturbances of membrane potential are Weak carried along the membrane 5331213339 1 l beige gt Local potentials degrade W time distance but are very fast diggtlggsa ggs gt Local potentials can add to produce an AP when encounter vd Na channel R x g gt Action potentials propagate down the length of an axon l i ll I Idea of successive patches of membrane each W vd Na 39 channels I SALTATORY CONDUCTION speeds up conduction velocity amp conserves energy ONLY need NaK pump proteins at nodes gt Conduction velocity is also proportional to axon diameter I AP s propagated down the axon gt Myelination lets smaller diameter axons to send signals quickly more axons in the brain gt In myelinated axons vd Na channels are gt concentrated at nodes of Ranvier i thpf l39jgng More axons can be placed in the brain q Myelln sheath 39 q Decremental Action potential conduction under is regenerated myelin sheath at nodes of Ranvier LECTURE 3 SNYPATIC TRANSMISSION How does an action potential pass on to the next cell encode the info I Electrical synapses gap junctions LESS COMMON in mammalian CNS gt Fast but in exible I Chemical synapse junction between pre and post synaptic components w a small gap gt Presynaptic is usually an axon I Axon terminal has mitochondria vesicles Golgi apparatus for recycling gt Postsynaptic component can be dendrite axodendritic synapse cell body axosomatic synapse or another axon axoaxom39c cynapse I Recently discovered dendrodendritic synapses gt Postsynaptic density thickening of the membrane lies under the axon terminal I Contains receptors for transmitters modulates its sensitivity I Transmitters can be put into and withdrawn from the membrane I Ribosomes are sent to the axons as they don t have ribosomes through Axoplasmic Transport transport along microtubules w aid of motor enzymes kinesin and dynein that is powered by ATP gt Can be anterograde AND retrograde terminals can send things back I NEUROTRANSMITTER RELEASE gt Vesicles lie near the presynaptic membrane gt Process I lArrival of AP at the axon terminal open vd Ca channels Ca is usually outside the cell like Na I 2Ca ions ow into the axon amp allows movement of synaptic vesicles to the presynaptic membrane that stimulate a fusion pore I 3 Fusion pore opens amp contents of the vesicle are released into the synaptic gap I Fusion pores don t open until there is interaction w proteins on the vesicular membrane I 4 The vesicles release NT into synaptic gap I ones that are closest are more likely to be released I released NT diffuses across cleft to interact w postsynaptic membrane receptors Cluster of protein molecules in membrane of synaptic vesicle Docked synaptic vesicle Cluster of protein in presynaptic membrane 1 77 r o 0 33 0 o o I 390 i 391 39 I I 39Iliiitiil M O C 0 O E l illustrators 0 Entry of calcium Fusion pore widens Molecules of Presynaptic 39 o opens fusion pore membrane of synaptic neurotransmitter membrane vesicle fuses with begin to leave presynaptic membrane terminal button Acetxl Choline mi I lndolamines I Serotonin mi Dogamine m I Catecholamines Noregineghrine I Noradrenaline Egineghrine I Adrenaline Glutamate most grominent in CNSI excitatogg l M l i H A l m GABA 3040 of CNS synapses inhibizoga Asgartate i What are neurotransmltters Glycinequot Neurotransmitters and m uanosme m neuromodulators can take ATP 7quot Others Endorphins Opioids Enkeghalins Dynorghins Substance P NonOpioids I E NeurogegtideY m Others many diff forms chemically I Amino Acids Glutamate and GABA I Neuropeptide string of amino acids What determines whether a NT is excitatory or inhibitory I Most can be both excitatory AND inhibitory I Depends on its receptors gt Receptors proteins in the membranes as the mechanism for recognizing the presence of a speci c signal I Postsynaptic Receptors gt Molecules of NT bind to receptors on the postsynaptic membrane I Receptor activation open PS ion channels I Ions enter the membrane producing either depolarization OR hyperpolarization I Resulting postsynaptic potential PSP depends on which ion channel is opened gt PS receptors alter ion channels I Directly ionotropic receptors brief fast I Indirectly that use 2Ild messenger systems that require energy metabotropic receptors longer lasting slow RECEPTOR BINDING TERMS I Things that bind to receptors ligand NT certain drugs hormones gt Ligands which stimulate receptor activity agonists I Ionotropic receptors are sometimes called ligandgated ion channels gt Ligands which do not stimulate activity just stops not actively stop antagonists I To be a receptor for NATURAL ligands gt When ligands binds to the receptor it should trigger a response gt Receptor is speci c the ligand gt Ligand binds to receptors reversibly gt MUST be some way to terminate action of ligand degradative enzymes in the synaptic gap break down NT I Every psychoactive drug works on either neurotransmitters or its receptors Ionotropic Receptors ligandactivated channel direct gating of ion channel usually of 45 subunits that results in a hyperpolarization of depolarization gt GABA 9 Cl nACh 9 Na ISIS Bijtr li lar 4 space V L d WhenACh l u y r I big 39 molecules oceupy 1 1 8 bth binding sit s I Site the sodium channel j opens 39 depolari zing the l postsynaptic cell c Reuptake Molecule of transmitter substance binds with 3947 produce 1 substance binds with 5 produce NE NE receptor postsynaptic receptor postsynaptic J Stimulatory Inhibitory 9 potential Ion Channe39 POtemia39 illecepm 2 receptor 2 Receptor a Re9eptor G39D O39ein Gpiotein activateS activateS I V a subunit messenger o G prOte39n gt a subunit breaks G pretem breaks away I 3 away binds with activates enzyme 1 To nucleus 3 protein b ion Channel and Wh39Ch prOduceS 6 or other parts kinaseA Opens it second messenger of cell Ions enter cell 39 Molecule of transmitter 39 Ions enter cell G protein opens G protein Adenytyl cyciase NW gt hm Siimulatory l Inhibitory a b LECTURE 4 SYNAPTIC TRANSMISSION cont Metabotropic Receptors recognizes the protein that then activates a secondary protein that then affects an ion channel or something else in the cell Common 2Ild messengers CAMP CGMP I Very common in the nervous system especially the brain AMPLIFICATION method potential for having a greater effect on the next cell in line Can open ion channels activate Tc factors that can change gene expression protein being made activate enzymes Ex Norepinephrine acting as its beta receptor stimulates the synthesis of CAMP while its alpha 2 receptor inhibits CAMP With interplay of excitation and inhibition both use energy can have a GRADATION gt Inhibition might be more important in some cases vision way that we see is inhibition Serotonin has 7 diff receptors 1 is ionotrophic the rest are metabotropic gt Some neurons can make certain neurotransmitters but are able send to many diff parts of the brain only 10 produces serotonin Actions of neurotransmitters at their receptors results in postsynaptic potentials gt Hormones and neurotransmitter both have a targeted area but hormones are in the bloodstream and neurotransmitter is packaged and released at the synapse both can be dopamine POSTSYNAPTIC POTENTIALS due to receptor activation are either excitatory EPSP or inhibitory IPSP I PSPS are conducted detrimentally along neural membrane gt Open Na ion channels results in EPSP gt Opening K or Cl ion Channels results in IPSP Neural interaction involves the algebraic summation of PSPS gt Predominance of EPSPSS reaching the axon hillock will result in AP gt If summated PSPSS do not bring the axon membrane pass the threshold no AP will occur Postsynaptic spatial summation synapses located on different part of the cells activate simultaneously multiple shovels to get AP Postsynaptic temporal summation the same synapse active over time one shovel to get AP gt Generally summation and temporal summation are both occurring NT receptors can ALSO be presynaptic inhibition or facilitation often by altering voltage dependent Ca via heteroreceptors presynaptic receptors that respond to NT released from adjacent neurons or cells they are opposite to autoreceptors which are sensitive only to NT or hormones released by the cell in whose wall they are embedded gt Presynaptic receptors are for feedback purposes that alter enzyme activity Emmlory Synapse 39 Two simultaneous EPSP sum to produce a greater EPSP A Slimmaled B Stxmulated A 9 8 Stirrmlated l 65 esLN 70 N 70 Two simultaneous IPSP39s sum to produce a greater IPSP C Simulated D Sumulateo C t 0 Simulated 39 esi A clmullaneouc IPSP and EPSP cancel each other out A Stunulatod C Simulated A C Simulated Membrane potential minivans i l To oscilloscope gt Two EPSP39s elicited in rapid succession sum to produce a larger EPSP m U 65 i 70 A39 quotA quot A quot Two IPSP elicited in rapld Iucceulon sum to produce a larger lPSP 65 65 Membrane potential mlltlvotts Axon o Neuron A 70 70 Axon Axon of Dendrite of Neuron C Neuron B Innninal Button i s a Voddos contain neurotransmitters Neuron D Neuron B Reuptake transporter Automcnptor Synoptic Clelt Neuron A a Presynaptic Facilitation Receptors Receiving Neuron b Presynaptic Inhibition How do we get neurotransmitter gt Peptide neurotransmitters are synthesized in the soma packed in the body and then transported gt BUT some are enzymatically synthesized SUMMARY at the synapse 1 Transport of NT or synthetic enzymes a Synthesis of NT b Packaging into vesicles 2 Ca entry triggers release into synaptic gap 3 Receptor activation 4 Postsynaptic potential 5 Autoreceptor feedback 6 NT inactivation reuptake or enzymatic degradation Drug serves as precursor AGO eg LDOPA dopamine Drug inactivates synthetic enzyme inhibits synthesis of NT ANT eg PCPAserotonin Drug prevents storage of NT in vesicles ANT eg reserpine monoamlnes Drug Stimu39ates aUtOI GOGPtOfS inhibits synthesisrelease of NT ANT I Drug stimulates release of NT 69 apomorphine dopamine AGO eg black widow spider venomACh Drug blocks autoreceptors increases synthesisrelease of NT AGO a Drug inhibits release of NT ANT eg idazoxan norepinephrine eg botulinum toxinACh Drug blocks reuptake AGO eg cocaine dopamine a Drug stimulates postsynaptic receptors AGO eg nicotine muscarineACh V Drug inactivates acetylcholinesterase Drug blocks f E I K AGO postsynagtIitlzTreceptors Molecules of eg physostigmine ACh eg curare atropine ACh drugs I Binding at receptors competitive or noncompetitive alters the shape gt Noncompetitive by binding at the sites they are being positive allosteric modulator GABA receptor I MOST GABA in the CEREBELLUM important for movement coordination balance LECTURE 5 6 ORGANIZATION OF THE CNS I Organization of the nervous system gt CNS brain and spinal cord conduit for info to and from the brain gt PNS cranialspinal nerves and peripheral ganglia I PNS nerves project to target organs and muscles efferent I Carry sensory info to the brain afferent gt Cluster of cell bodies in CNS nuclei cell bodies in PNS ganglia Sympathetic i I Touch is aware somatic 39rquotr Parasympathelic nervous system NEUROANATOMY TERMS I Neuraxis imaginary line drawn the length of the spinal cord up to front of the brain I Anatomical directions relative to the neuraXis gt Rostral toward the head 9 OW Dorsal Rostral or Caudal or 39 I an erior sterior Lateral lt gt Lateral gt Caudal toward the tall 9 Medial mm gt Ventral toward the belly V I I gt Dorsal toward the back Dorsal Bursa Rostral or gt Medial toward the neurax1sm1d11ne 34 News Lateram gtLateral gt I Medial gt I lt Medial Lateral away from the neuraxismidline I For people gt Anterior toward the front face gt Posterior toward the back gt Superior top of the head gt Inferior bottom of the feat I LeftRight location on body gt Ipsilateral same side gt Contralateral opposite side l I Close Proximal 9 Away from center Distal Caudaw Caudal or posterior posterior Ventral Ventral 198100 PLANES OF SECTION brain can be sectioned in three planes I Each section is a diff 2D view of the internal anatomy of the brain gt Sagittal right and left division gt Transverse Coronal frontal front and back division gt Horizontal transaxial top and bottom divisions Dorsal 39 39 A b d 39 T I J g g ransverse p ane frontal section 39 39 v Vl Horizontal 7 Sagittal i o I plane plane I 3 Ventral I Z 7 7 Dorsal y 5 i 39 I 7 1 t 4 7 Ti mi i l I Rostral V L A Caudal 39 3 quot yr 4p t i r u 1 i r 7 Transverse plane Ventral cross section l j l i l x Rostral H 9 r I F 7j l Y X s J h a Caudal Ventral Lateral ventricle I xr 33914 c The Dura Mater B 1 gt Skin of scalp A Periosteum Bone of skull Periosteal Dara Meningeal mate Arachnoid mater Pia mater Arachnoid villus Third Blood vessel ventricle Superior sagittal Sinus Subdural space V 5 Subarachnoid space Falx cerebn Massa N intermedia Cerebral aqueduct Fourth ventricle Brain spinal cord are protected by 3 layers of membranes MENINGES I 3 layers gt Dura mater outer thick layer and is responsible to keeping the cerebrospinal uid I Major veins are here gt Arachnoid mater I Overlies the subarachonoid space CSF space between arachnoid membrane and pia I Blood vessels run through the arachnoid gt Pia mater inner thinnest layer I Overlies every detail of the outer brain I Subarachnoid space lled w Cerebrospinal Fluid CNS develops from a hollow tube and remains hollow gt Brain oat in a pool of cerebrospinal uid CSF contained by the meninges which cushions it gt CSF is also contained within 4 brain ventricles and spinal central canal gt CSF and the ventricular system I CSF is produced by the choroid plexus complex of specialized blood vessels in the ventricles I CSF and ventricular system can ALSO be an access point for the chemical measurements or stimulation I Brain ventricles can expand when brain cells are lost lost of nerves far too fast for astrocytes to take up the space that is exposed alcoholism schizophrenia CNS organization from a developmental perspective NS develops from the outer layer ectoderm of the embryo and forms a plate of cells I Growth of cells along the midline grows faster than other cells which cause a mound that becomes the neural tube gt Comes to a point and is shut from rostral 9 caudal I Developmental defect can result w Spina bifida A I By day 28 rostral end of the neural tube has formed ventricles I By day 36 tissue that surrounds the ventricles form the 3 major divisions of the brain F orebrain midbrain hindbrain Neural groove Forebrain Midbrain Hindbrain Telencephalon Mesencephalon Cerebral Paraxial hemisphere mesodetm Metencephalon Thalamus 4 r Myelencephalon Rostral Caudal a Diencephalon Hypothalamus b Pituitary mesoderm gland M39db 39 Cerebral Basal Thalamus B 39Pra39n cortex ganglia rain OnS Dorsal Tecmm Stem Medulla Cerebellum plate mesoderm A Cerebellum Spinal cord Medulla e Ventral D C Spinal Hypothalamus Tegmentum Pons cord 039 11 a Development of the human brain Midbrain b Organization of the adult human brain 6 mais s snozuau sq yo suogsyi Telencephalon Cerebral Erebellum hemisphere Hindbrain Neural tube Forebrain Diencephalon 39 39 25 days 35 days 40 days 50 days 100 days Telencephalon cerebral hemispheres H x t 1 I iV Ua vquot in Basal ganglia n39 in 9N3 mais s snouau exiuag Adult brain 214 Divisions of the Human Nervous System in the Embryo and the Adult 2 A few weeks after conception the head end of the neural tube shows three main divisions Seven weeks after conception five main divisions of the brain are visi ble b A schematic depiction of their organization and c the positions of these divisions in the adult brain maas s snouau 913W dyad Te39e cepnal Pr met xtgx mhm Rxcxaml Dmncepna39oa 9k39rmu39e5i h1laui llmtxaml BRAIN DEVELOPMENT AND ORGANIZATION thomm Mvelelvsophaorn on Myelencephalon compose of the I Medulla MOST caudal part of the brain and is rostral to the spinal cord Spmm com I gt Contains part of the reticular formation and ascending and descending pathways I Is a continuation of the spinal cord gt The nuclei of the medulla control vital functions such as regulation of the cardiovascular system breathing and skeletal muscle tone gt Home for a lot of the re exes I Damage in the myelencephalon inhibits life functions and can result in death Metencephalon consists of the I Cerebellum involved in motor coordination amp skill learning gt Large of pathways enter eXit the cerebellum ones that don t continue onto the pons Rolleular gt Big computing system whose output is down to the spinal cords 39 quot39quot quot gt Unconsciously coordinates sequence of movements sent by the motor corteX for FAST movement I Pons core of the reticular formation detects change the alertingarousal system game gt Involved in sleep and arousal super39orcm39mu39us Dorsal Cerebral Mesencephalon midbrain consists of Reticular aquedum I Tectum dorsal potion of midbrain formation Red gt Superior vision and inferior hearing location colliculi are 39 I nuc39eus involved in sensory systems gt Periaqueductal gray in involved in pain modulation I Tegmentum is the portion of the midbrain located ventral anterior to the tectum and consists of the gt Rostral end of the reticular formation gt Red nucleus filled with blood vessels gt Substantia nigra black tissue in fresh tissues the cell bodies have 3333mm pigment produce a lot of dopamine I Die off in Parkinson s disease neurological diseases that causes motor dysfunction gt Ventral tegmental area dopamine neurons that are involved with reward Diencephalon consists of Corpus Massa Wallofthlrd I Thalamus contains nuclei that receive sensory info except for smell mm mm mlmed39a View and transmit it to the corteX I Hypothalamus cell groups nuclei involved in integration of species typical behaviors control of the autonomic nervous system and pituitary gt Determines which hormones the pituitary will release V Iquot gt Coordination of hunger gt Posterior pituitary develops from the diencephalon C A Ventral I Hypolhalamic 5 Marnmlllary nudei I Optic chiaem gland Fornix Telencephalon is comprise of Subcortical structures such as the limbic system and basal ganglia gt Limbic system I Hippocampus declarative memory I Amygdala emotional memory I Mammillary Bodies diencephalic located in the hypothalamus I Their connection and relays eg the fornix is a pathway that connects the hippocampus with the mammillary bodies gt Basal ganglia subcortical nuclei that lie just under the anterior aspect of the lateral ventricles amp dorsolateral to the thalamus I Involved in the coordination of movement affected by Parkinson s and Huntington s disease I Consist of part of the brain that loses input when the cell bodies die off Globus pallidus Caudate nucleus Putamen gt The cerebral cortex neocortex and allocortex body CEREBRAL CORTEX neocortex outside new and allocortex inside old forms the outer surface of the cerebral hemispheres 3 Par sulcus l sulcus Primary auditory Portion of Left Hemsphere Lateral fissure gt Sulci small grooves and gyri outer protrusion Fissures large grooves 4 lobes front parietal occipital and temporal lobe composed primarily of cells gray appearance Neocortex is formed from 6 layers of cells Granule cells are input neurons and pyramidal cells are for outputs 0 In general external layers deal with telencephalic parts of the cortex inputs and outputs 0 Internal deal with extratelencephalic connection outside of the telencephalon PRIMARY SENSORY AND MOROR CORTEX I Primary somatosensory cortex sensation from parts of the bodies I Primary motor cortex movement of parts of the body gt Primary motor and somatosensory cortex separated by the central sulcus Primary somatosensory cortex Right W Hemisphere iquot Feet Eeet Calcarine Trun Trun fissure y H C x 5 ire w 39 E 5 i Primary motor cortex Central sulcus ands Ha Fing s ace Face Lipo Lip Figer Primary visual cortex 4 AV amp my lt A 7 Primary auditory cortex Left Hemisphere Mammillary Hippocampus Massa inlarmedia belween two lobes of thalamus Hippocampus of right hemisphere ghosted in Globus pallidus Molecular layer External Granular layer External pyramidal layer Internal granular layer Internal pyramidal layer Mutifarm layer 5 Limbic cortex Caudate nucleus and putamen 9 GlamWvuwal l B Alame JLI MIV Tail of caudale nucleu Q Upper Motor Neurons lie Cewical the spinal card MAJOR INPUTS AND OUTPUTS OF THE BRAIN cranial nerves T quotquot 39 spinal cord I Spinal cord gt All mammals if not counting the tail has the same of vertebrae 39 spinal nerves that as humans 321222 gt Spinal column grows longer than the spinal cord Lumbar gt Anatomy of the spinal cord in the cerebral cortex gray matter 0mm m surrounds white BUT for the spinal cord the white matter q surround the gray I Autonomic Nervous system sympathetic leave from thoracic and samequot lumbar part of the spine vs parasympathetic leave from brain and the sacral part of the spine The spinal cord ends between LI and L2 The nerves gt D ifferent continue to descend in the spinal column exiting between the vertebrae and through the sacrum I Functionally Anatomically Chemically diff NT and receptorS To brain Dura mater Dorsal I Dorsal section more sensory function autonomic root Afferent axon I Ventral section more motor function somatic 33372 Arachnoid membrane Pia mater Dorsal white column Dorsal median sulcus 7 From dorsal root VS gray horn Somatic Lateral Lateral sensory afferent white lt gray horn Visceral column sensory Ventral h Visceral Vemral 39 a J Spinal ray om motor root 39 nerve efferent Somatic motor Efferent Ventral ventral axon Motor Spinal Subarachnoid Fat tissue Vertebra hite commissure gray neuron cord space for cushioning ommissure To ventral root I Ventral Ventral White COIUmn median fissure Preganglionic axons Postganglionic axons l Pupil l l u i 1quot Cranial nerves 12 pairs Cervical nerves 8 pairs Thoracic nerves 12 pairs 391quot 39 39 Small intestine Lumbar 39 Large intestine nerves y f r r 39 t st ganglia 39 K Sacral nerve 5 pairs 39 Coccygeal nerve Parasympathetic outflow 1 pair Cenitals Sympathetic outflow 1I LECTURE 7 8 SENSORY SYSTEMS What does a sensory system have to do I Discriminate among diff forms of energy intensity rapidly I Convey this to the CNS we of sensory system Modality Adequate stimuli CLASSIFICATION OF SENOSRY SYSTEMS Mechanical Touch Contact With or deformation of body surface Principles for sensory processes Hearing Sound vibrations in air or water I Transduction of physical energy 9 neural activity V9 quot quotquot He ld quot 0me and mam Jornt Position and movement gt Accomplished by a spec1al1zed receptor or by a Muscle Tension specialized ending on dendriteaxon photic Seeing Visible adiam emgy gt Spec1ahzed receptor Thermal Cold Decrease in skin temperature 39 Receptor potential Warmth Increase in skin temperature 0 Graded Chemical Smell Odorous substances dissolved in air or water in the nasal caVity Leads to transmltter release 39 Taste Substances in contact with the tongue or gt Specialized ending other taste receptor 39 Generator potential Common chemical Changes in C0pH osmotic pressure 1 Vomeronasal Pheromones in air or water Leads dlrect y to AP Electrical Electroreception Differences in density of electrical currents Sensory coding theories I Muller 1835 law of speci c energies become spatial code or modality specificity ll theory 2 gt Nature of perception is defined by the pathway over which the sensory info is carried gt Difference in perception are not caused by differences in the stimuli themselves but by the different nervous structures that these stimuli excite I Temporal code info on intensity of stimulus gt More intense a stimulus the higher the rate of APs and patter of ring I Topographical organization within a sensory system and within the CNS VISION Visual stimuli wavelength 9 hue intensity 9 brightness purity saturation I Pupil opening that allows light to pass through I w focuses the light on the retina gt Shape altered by contraction of the ciliary muscles I Retina back surface of the eye that is lined by visual receptors gt Light from top strikes bottom lights from left strikes right and vice versa I Sclera whiteopaque that does not allow transmission of light Muscles focus the lens Muscles move the e e y Eyebrow Sclera 39w 0 elid a y Eyelashes Cornea Anterior chamber Optic nerve Blood vessels Lower eyelid Vitreous chamber 2010 Cengage Learning xtraocular muscles 139 I Interneurons are bipolar cells I Light interacts w photopigments in the Light receptors cones and rods and ipRGCs intrinsically photosensitive retinal ganglia cells I Retina Rods 120 mill Cones 6 mill gt Rods sensitive to intensity but not to wavelength gt Fovea sharpest vision mostly cones 9 daylight color 92010 Cengage Learning Lights inhibits rods and cones Hyperpolarizing Depolarizing Recording membrane membrane of action potential potential potentials Stimulus Photoreceptor ltl Light Ganglion To brainl cell Light passes through retinal neurons to visual receptors Axons of optic nerve Ganglion cell layer Inner plexiform layer Inner nuclear layer Outer plexiform layer Outer nuclear layer cell Layer of photoreceptor outer segments Rod Pigmented epithelium Toward the center at the eye it ll Away from the center of the eye Low Convergence In ConeFed Circuits Retinal Bipolar Cone ganglion cell cell High Convergence In RodFed Circuits Retinal Bipolar Rod ganglion cell cell gt In dark photoreceptors release NT depolarized light hits which hyperpolarizes it decrease amount of NT I Photoreceptors are NOT neurons yet can release NT gt bipolar cells receive input from visual receptors photoreceptorsgt ganglion cells receive input from bipolar cells start AP gt Interneurons amacrine amp horizontal cells exchange information with neighboring neurons Optic nerve is made up of ganglion cells axons Horizontal cell Amacrine cell Axons from ganglion cells Cantulinn rnllc Optic nerve 1A Region of overlap Visual lield of two visual lields of right eye r x x Optic chiasm VISUAL PATHWAY I Retina axons from ganglion cells in the nasal half of the retina 33132quot quot quot cross those from the temporal half do not 12 ipsilateral 12 visual field green contralateral Visual held I II Lateral geniculate nucleus of thalamus end of geniculate axons 39 mm A Superior colliculus Opmewe III Visual cortex 5236 nucleus GENERAL SYSTEM PRINCIPLES 1gg jfquot m W I In human visual system 50 of the ganglion cell axons cross at visual field yellow visiTaalry optic chiasm but input to the visual cortex is almost completely from contralateral visual eld I Topographical organization fovea is small part of retina but foveal input is 25 of primary visual cortex RECEPTIVE FIELDS what is it exactly that a neuron in a sensory systems responds to receptive fields based on location vary by size I Where does the stimulus have to occur to alter not necessarily excite the response gt In the center excites gt In the surrounding area inhibits gt Outside of the surrounding area does not alter it it will still continue to randomly produce AP I Excitatory and inhibitory can help pinpoint exactly where the stimuli is I Retinal Ganglion cells have circular receptive elds foveal fields have smaller fields than peripheral cells 0mm we gt 2 parts a circular center receptive field center ONa39ea OFFa39ea and a surround w an opposite response ortaroa ONaroa A Chen I Ganglion cells process visual info in 2 parallel poienvms pathways comer Surround Light Ugm gt Oncenter ganglion cells low baseline activity firing during light at center surround light 139355t1e 3quot gquot ggeplive gt Offcenter ganglion cells low baseline activity I inhibited by light at center excited by light in m l HMl H MHWH surround gt BOTH show a brief response to end of stimulus 0 big LO S o blitz LO 5 How do we discriminate among wavelengths of light a m COLOR VISION THEORIES color mixing is NOT pigment mixing I Trichromatic theory argues that there are 3 diff receptors that overlap w each sensitive to a single hue gt BUT can t explain the afterimage effect Blue 419 496 531 559 nm 10 quot 8 g 2 O 3 1395 E 05 g 0 o Red lgm Green hghl Stimulates stimulates 39reo cone green39 ccne Red on Green on green off red off 1 l I Opponent theory notes that people seem to perceive 4 primary colors y gt Yellow as a primary color rather than a 2 mixture of red and bluegreen light i Yellow on blue off Blue on yellow off I Negative color afterimages suggest that r g are complementary colors as are blue 90 VCIIOW lighl stimulates 39red and 39green cones eQually i A AA A AA 0 7 ll Ec r 399 Blue light stimulates blue cone iXi 399 and YCHOW Ziggy 3311garlqixuncnli ngmcn gungmn aquot Yei39owbluugangllonccli Y l039blurginghamcal gt Primate retina contains 3 types of 39539quotquotquot quotquot mm quot quotquotquotmm WS PhOtOFCCCPt0r5 Egl ltliquot i i I Each cone uses a diff opsin which is It Icl 39039 sensitive to a particular wavelength br g supports trichromatic theory gt At the ganglion cell level the system responds in an opponentprocess system gt ALL colors are combinations of I Yellow or Blue PLUS red or green I Pure red is not a thing as when red is stimulated RG says RED while BY says YELLOW so blue cones must be stimulated so it cancels red in BY channel leaving only the RG channel quotKillTiliilg liiiiiiii1323 B quoti im1 Lquot iq 139j5 quot 3 Bi 539 cancel each R G other out nothingy and S not R G and Al 339 L are not 0000 O R G stimulated 2 red gets nothing nothing c c c External ganular layer External pyramidal layer internal granular layor Hamel pyramidal byer B r layer stimulated blne B Y stimulated 2 blue R G stimulated red inhibited yellow inhibited 39 ll0 inhibitec 2 green inhibited o reen Striate Cortex V1 is organized into 6 layers contain nuclei and dendritic trees gt Layer 4 receives info from all layers of the ipsilateral LGN and is L 39 l 39 39 o 39 4339 l quotKl39ztis39l3 i39I gt Ntul mm moetLGNlnputs pi t 39ZWN 14quot 7 2 quot 3995 5 Cytochrome oxidno 39 Tail or39 1 Receptive field of a simple cell exceptionally thick y gt Visual info is sent to layers above and below layer 4 for analysis 39 Off area I Microelectrode receptive field studies have sought to identify the V features of the external world that activate cells in striate cortex 39On39 area gt Orientation sensitivity some cells fire best to a stimulus of a 2 Bar 35ng particular orientation and fire less when orientation is shifted 39 Lht 39 Lg I Why would this be Helps define edges 61 3 cl l I Neurons are NOT responding to light light rodscones beg ganglia LGC Simple cells of primary visual cortex 0 H b lO H gt Cortical receptive elds are the product of their inputs and look d l diff from ganglion receptive elds M o o o axnmally gt LGC do have receptive elds but it layers the mfo sent by effecting w Hlllll c S ImU U oppos1te retma and the 1ps11ateral retma f Diffuse gt VI receives input from both eyes via the LGN in alternating 9 39quotum39nat39on columns o 1 2 3 sec h gii Horizontal section 0 1 2 3 sec of striate cortex V B e 5 I Laterall t gglrl l cu a e Simple cell of I I II II 1 Q Perimeter of visual areas Dorsal stream Where Area MT oArea MST Area V2 Extrastriate cortex Striate cortex 6 3 39 Pathways to the secondary Visual cortex Dorsal stream 1 Ventral stream and ventral stream who or what pathway separation WE V4 begins at the LGN I I I I I Area IT I Visual secondary or ass001at10n cortex Visual info is l transmitted to extrastriate cortex sometimes termed visual association cortex via two pathways gt Dorsal stream where and movement of object I Derived from more magnocellular input LGN layers 1amp2 gt Ventral stream who or what analysis of form I receives an equal mix of LGN magnocellular parvocellular and konicellular g intralaminar input I project to extrasrtiate cortex and to inferior temporal cortex I Disorders following brain damage gt ventral stream I Prosopagnosia is inability to visually recognize familiar faces and some objects I Caused by damage to the inferior temporal cortex part of the ventral stream including the fusiform face area gt Dorsal stream I Sensory neglect is ignoring of sensation from side of the world contralateral to damage I The posterior parietal cortex combines input from the visual auditory and somatosensory areas to help the individual locate objects in space and to orient the body in the environment 10 Dermatomes 5 segments sewed by a 3 spinal or cranial nerve u 39 1391 7 quot LECTURE 8 cont SOMATOSENSES body senses provide 3 I I i 1351 info relating to events on the skin and occurring within the 3 body l Mm I Skin cutaneous sense receives various signals from the 25 skin that form the sense of touch ca3939 twmmwum MN gt Pressure Temperature Stimuli that damages tissue quot Ili i39f iffi1175332213 1252 339 quot quot quot39quot gt Cutaneous senses Diff sensations are reported to the gA brain by neuronal endings within skin and they 7quot follow diff pathways to the brain 52 z I Proprioception kinesthesia provides info about the body 82 position and movement us gt Kinesthetic signals arise from receptors located u quot within joints tendons and muscles 839 I Interoceptive system is concerned w sensation in our quot 39 internal organs I Each follows a diff path in CNS and within can arise from diff parts of the body Morphology of Skin there are 2 general types of receptors in the skin Free nerve endings are processes at the ends of neurons detect warmth cold and pain All other receptors are encapsulate receptors more complex structure w specialized endings gt Their roles is to detect aspects of touch Density of skin receptors type vary gt Hairless glabrous skin is MOST sensitive I Meissner s corpuscles are only found in glabrous skin I Merkel s disks are also for fine touch and texture but are in both hairy and glabrous skin TABLE 73 Major Features of the Mechanoceptors Mechanoreceptor Meissner s corpuscles Pacinian corpuscles Merkel s disks Ruffini s endings Encapsulated Yes Yes No No Size of Receptive Quality of Stimulus Rate of Adaptation Field Sensed Rapid Small Pressure Rapid Large Vibration Slow Small Pressure Slow Large Stretch Cutaneous Senses Diff sensations are reported to the brain by neuronal endings within skin and they follow diff pathways to the brain Touch involves perception of pressure vibration of an object on the skin gt Involves activation of special ion channels that respond to physical energy transient receptor potential TRP channel family of proteins gt Afferent AP then travel to CNS Dorsal columns Touch Sensory info does not cross until its gets to the brain gt Not contralateral until the 2ND neuron in the circuit in medulla Skin AP 9 Spinal dorsal columns white matter 9 medulla crosssynapse 9 Ventral posterior thalamus9 Postcentral gyrus primary somatosensory cortex Pacinian corpuscle Hairy skin Glabrous skin gt Epidermis Merkel39s g u disk 39 39 quotquotquotquotquotquotquot quot Free nerve in end 9 Dermls Meissner s corpuscle Hair follicle s receptor quot Subcutaneous ssue Pacinian l corpuscle Ruffini39s ending OZOI 0 Cangage Learning otte Cerebral cortex postcenlral gyrus o in 111 Vem ricle 395 5 Forearm and hand area Qf g 39 a Thalamus J l Head Face A I f le ll NeuronIlI In Internal n capsquot 5 l capsule post limb Lenticular nuc Vent posierolateral nuc Medial lemniscus Medulla Nuc gracilis Nucl cunealus Medulla 39 Spinal nuc of N I Neuron II internal quot arcua le fibers Decussaiion of medial Dorsal root ganglion ce lemniscus fibers Neuron I 39 x I Unencapsulaled 74 h aquot joint receptor a quot o quot LIII GolgiMazzani N4 39 corpuscle Q Fasciculus cuneaius Fasciculus gracilis What about other cutaneous sense like pain and temperature There is no specific neuron for it Diff sensations are reported to the brain by neuronal endings Within skin and they follow diff pathways to the brain Temperature is detected by free nerve endings gt The endings rely on diff transient receptor potential TRP channels and lie at diff levels of the skin cold are close to the surface of the skin Pain detection requires several receptors based on type of pain gt Mechanical pain receptors have not yet been identified gt Chemical pain the TRPAl receptor accounts for the pain caused by tear gas tobacco smoke and some foods gt Thermal pain TRPV1amp2 receptors respond to painful heat I RTPV2 also responds to capsaicin found in chili peppers Sharp pain by fast myelinated axons and dull longlasing pain by slower unmyelinated fibers gt Temperature and pain travel in the lateral White matter Lateral spinothalamic tract Cerebral cortex postcentral gyrus 0v c Corpus callosum 0 Axon of neuron in posterior limb of internal capsule Thalomus Internal capsule Vent posteroloteral quot nucleus Mldbrain Substantia nigra Crus cerebri Pons E 0 J quotb c7 Medial le mniscus Hquot l g39 5 1 42 6 MwW Reticular formation Medulla Lateral spinothalamic tract Neuron I i J dorsal root ganglion cell k39m 0 Sacral fibers Temperature u I l A r 0 Lumbar fibers PM 39 ZThorucic fibers 39 cm quotWmquot mumw Cervical fibers Pain receptors free nerve 39 endings in skin of O D I t I f I dermafomes 1 3 orsoo era ascrcu us cm and T11 quot quot zone of Lissauer e c d recepm iquot Cells of substantia gelatinosa 5km 0f dermalome and nuc centrodorsalis LIiI 6 Axons crossing to opposite Heal receptor quot1 U side in anteriorwhite commisure skin of dermatome E 39 SI 39 Body Senses somatosensory system share a of features W other sensory systems The area devoted to a part of the body corresponds to the sensitivity of the body part Somatosensory processing is hierarchical primary somatosensory cortex secondary somatosensory cortex parietal temporal lobes The secondary somatosensory cortex receives input fro m the left and the right primary somatosensory cortices so it combines info from both side of the body gt Neurons in this area are particularly responsible to stimuli that have acquired meaning like association w reward gt 2Ild somatosensory cortex concert to the part of the temporal lobe includes hippocampus I hippocampus may help determine Whether a stimulus is committed to memory Posterior parietal cortex association area that brings body sense vision and audition together gt Brains decided body s orientation in space location of limbs and location in space of objects gt Serves cross modality transfer 391 LECTURE 9 CONTROL OF MOVEMENT Strategy tactics execution I Motor Cortex gt Multiple motor systems control body Somatosensory cortex feedback from muscles and tendensl 1 Primary motor cortex controls voluntary movements Dorsolateral prefrontal cortex and secondary motor cortex planning and preparation for movement Posterior parietal cortex visual auditory and somatosensory informatan l h Basal ganglia Cerebellum selects and integrates gt Brain stem coardinates skilled movements movements action gt Primary motor cortex is located on the 1 precentral gyrus I Motor cortex is somatotopically Cm S quot nerves spinalnerves organized motor homunculus gt Planning of movements involves the premotor cortex and supplemental motor areas which in uence the primary motor cortex I Motor Homunculus parts of the body used in requiring precision and fine control such as face and hands have disproportionately large representations in the motor map gt Size of primary motor cortex remains constant across phylogeny in y proportion to body weight Motor cortex receives input from Premotor cortex pre SMA Supplemental motor area 0 Primary somatosensory cortex Prefrontal cortex executive fx w input from pose parietal Movement Butlocks Genitals BUT the topography homunculus varies W specialization Jaw Swallowing Primary somatosensory cortex Supplies motor areas with information about the body such as limb position Primary motor cortex Executes movements Posterior parietal cortex Supplies motor areas with information about location of body parts in relation to objects in space Supplementary motor area Assembles sequences of movements Premotor cortex Combines information needed f0r movement begins programming Prefrontal cortex Holds in memory information abOut the world and about the body while selecting appropiate movement and target Cerebellum Contributes order and timing to intended movements sends information back to motor cortex Secondary Motor Areas supplementary motor amp premotor cortex also inputs to primary motor cortex from basal ganglia via ventral anteriorlateral thalamus gt Damage to secondary motor areas 9 inability to coordinate hand and digits apraxia not paralysis gt Apraxias inability to properly execute a learned movement following brain damage Limb apraxia involves movement of the wrong portion of a limb incorrect movement of the correct limb part or an incorrect sequence of movements 0 Frequently follows premotor area damage Constructional apraxia difficulty in depicting 3d objects right parietal lobe damage 39739 I The Basal Ganglia consist of the caudate and putamen striatum and the globus pallidus gt Input to basal ganglia from PMC and substantia nigra but also cerebellum and somatosensory cx gt Output to basal ganglia is from globus pallidus to I Thalamus motor cortex and brainstem motor nuclei red nuclei vestibular nuclei gt Use sensory input to guide slower movements learn rules and organize sequences into a smooth automatic whole I Organize action sequence into chunks or units like learning to drive a car habit learning and inhibits extraneous movements I Linked to obsessivecompulsive disorder repetitive thoughts and actions that the person knows are pointless I 0CD patients have increased activity in caudate nucleus which is reduced w effective treatment Giobulus pallidus Thalamus Head of Tail of caudate caudate nucleus Amygdala nucleus Substantia Nigra Caudate Putamen striatum Striatum Globus pallidus Basal ganglia I The Cerebellum consists of 2 hemispheres w associated deep nuclei gt Important for balance posture motor learning and rapid movements compensations gt Damage to the cerebellum results in jerky erratic and uncoordinated movements de cits in motor skills particularly the timing of movements Divisions of the Cerebellum a Caudate nucleus Putamen b Midbrain Internal capsule Thaiamus Spinocerebellum Primary fissure Vermis Hemisphere Intermediate part d of hemisphere 3 Lateral part of hemisphere A a Anterior lobe Anterior lobe Spinocerebellum Posterior lobe Flocculus Medulla 3 TWO 9 cerebellar hemispheres m Fioccuionoduiar lobe Flocculus 7 392 Vestibulocerebellum DESCENDING MOTOR PATHWAYS primary output from motor cortex in the pyramidal tract which as both a corticospinal and a corticlbulbar component I Doesn t go contralateral until the caudal portion of the medulla appendages fine movements and ventromedial or anterior more for trunk and posture gt Neurons of the corticospinal tract terminate on motor neurons within the ventral horn of the spinal cord I Corticospinal tract starts primary motor cortex I Descends through various white matter areas of the brain I Corticospinal neurons decussate crossover in the medulla I at the medulla 80 switched to contralateral while 20 stays ipsilateral I the 20 that stays on the same side requires less motor neurons I Terminate on motorneurons of ventral horn gt Motor neurons neuron that sends info out to a muscle motor neurons are within the ventral horn of the spinal cord I Descending pathways in the spinal cord gt divided into a lateral group lateral corticospinal amp rubrospinal and a ventromedial group lateral corticospinal rubrospinal medial vestibulospinal tract tectospinal tract medullary reticulospinal tract pontine reticulospinal tract anterior corticospinal tract lateral ves bulospinal tract Some movement disorder Corticospinal Pyramidal tract 2 descending components split at the medulla lateral for Hand Face rr39l Tongue f l Basal ganglia r 39 A7Thalamus f 9 Internal J quot capsule MIDBRAIN CerticobUIbarlract LOWER MEDULLA 39 233quot Pyramids SPINAL CORD Lateral corticospinal l Anterior corneospmal 7quot tract MOTOR PATHWAYS CORTlCOSPINAL AND CORTICOBULBAR TRACTS Parkinson s disease characterized by motor tremors rigidity loss of balance and coordination and difficulty in moving especially in initiating and stopping movements gt Symptoms are caused by deterioration of substantia nigra cell bodies and the loss of the dopaminergic input to the basal ganglia I Most treatments target dopamine ldopa 71 Awa ke wAlMiM39rA39WIIquotlNI39Vw WWVWMM WMWMWWMquotWWWNWW Alpha activity Beta activity Stage 1 sleep LECTURE 10 and 11 SLEEP What is sleep I A behavior and an altered state of consciousness Stage 2 sleep gt Few movement occur during sleep WWWVva KVWMWWNWWWWM I Nature of consciousness is changed during sleep recall little 3356 Kcomplex Seconds mental activity during sleep anterograde amnesia I 13 of our lives are sleeping Stages Sleep gt What happens mlAiquotmVWMWMM MN gt What are the functions of sleep V gt What are the neural mechanisms How is it related to our circadian rhythms Measures of Sleep electrophysiological instruments can be used in kfx the sleep laboratory to assess the physiological changes that occur i i during an episode of sleep De39ta actiVity I EEG summated brain wave activity assess brain activity REM sleep gt Alert beta activity 1330 Hz I Desynchrony low amplitude high frequency wavelengths gt Eyes Closed al ha activity HZ FIGURE 92 An EEG Recording of the Stages of Sleep I Synchrony high amplitude low frequency waveforms I Muscle tone EMG calcium entry I Eye movement EOG I Heart rate blood pressure and blood ow under the in uence of the ANS I Stage of Sleep 14 nonREM amplitude increase as wave slows down Alert Beta 1330 Hz Stage 1 bursts of theta activity lt10 Hz Stage 2 sleep spindles bursts of delta activity Stage 3 Delta activity lt3 HZ 2 30m Ogdeep Stage 4 Delta activity HR BP body temp decreases I After 90min EEG starts to speed up back to beta activity gt REM paradoxical Beta activity loss muscle tone during REM sleep most likely to report a dream I Sleep onset progression through all 4 stages within 3045 min gt NonREM parasympathetic activity predominates gt 90 min after sleep onset REM and sympathetic activation gt Subsequent cycles more REM less SWS slow wave sleep I Dream episodes usually correspond to REM episodes content could be in uenced by external events and timing gt REM sleep is accompanied by high levels of bloody flow in the visual association cortex but low levels in the prefrontal cortex gt Dream content most are about routine life maybe brain s attempt t 0 make sense of random neural activity gt Major exceptions hypnagogic relating to the period of drowsiness just before sleep experiences in Stage 1 and sleep terror during stage 3A SWS WW I REM and PGO Spikes slightly precede EEG Geniculole desynchronization and REM I Starts in pons lateral geniculate nucleus occipital Delta activity Stage 4 sleep Theta activity Beta activity VVVVV Occipitol cortex Pons 7 What is the function of sleep I Sleep as an adaptive response gt Sleep is noted in ALL vertebrates gt Signs of REM sleep muscle paralysis EEG desynchonry eye movements occur in mammals and birds I Restoration and repair gt Brain activity is reduced somewhat during SWS delta activity is slow but synchronous Less muscle activity gt Only somewhat in uenced by level of activity so many CNS waste removal I Increase in tiny glial regulated channels of CSF cerebral spinal uid and removal of potentially neurotoxic compounds from the brain during sleep I Effects of sleep deprivation gt Hallucinations REM state intrudes upon the waking state gt Animal studies indicate drastic health consequences of sleep deprivation I Sleep deprived rates eXhibit increased eating W WWW EEG refill activity and eventually fall ill then die gt Human sleep deprivation studies indicate that sleep deprivation can affect cognitive function I Perceptual distortions hallucinations and increased irritability are reported during sleep B Experimental animals Experimental rat Wle EEG 0 7 14 21 28 Days of sleep deprivation Death Figure 273 The consequences of total sleep deprivation in rats A In this apparatus an experimental rat is kept awake because the onset of sleep detected electroencephalographicallv o o o o triggers movement of the cage floor The control I C ogn1t1ve 1mp a1rments 1nclude concentration mt brown the sleep mtermmenuy p i v whereas the experimental animal white cannot o o t g B After two to three weeks of slee d 39 r 39 4 m s o I p eprn ation r f m e m the experimental animals begin to lose weight i 39 quot floor fail to control their body temperature and even tually die After Bergmann et al 1989 I Sleep deprivation also inhibits leptin and stimulate ghrelin I Immune suppression w continued deprivation I New memory formation also impaired I SWS may re ect restoration and recovery gt Mental activity and exercise small increase in SWS gt Growth hormone release is increased during stage 34 gt REM can be deprived but if you deprive SWS it comes w depriving of REM sleep I REM as a period of integration of neural activity w previous eXperience gt Facilitation of brain development Infants spend more time in REM sleep gt As increase in age there is less NREM and REM sleep I SWS is more critical for establish factual memory and REM for procedural and skill memory Multiple functions of sleep Energy conservation niche adaptation physical restoration memory consolidation and neuroplasticity relative importance of each may vary with species I Control of sleepwaking gt Sleep is regulated lost of sleep is made up but only somewhat on following nights rebound or recovery gt Unlikely that sleep is completely controlled by bloodborne chemicals hormones in the general circulation give that I Conjoined twins share the same circulatory system but sleep independently I Bottlenosed dolphins 2 hemispheres can sleep independently Neural regulation of arousal electrical stimulation of the cholingeric cell groups in the dorsal pons and basal forebrain induces arousal by projection to cerebral corteX I Other NT systems involved in arousal and sleep 7A gt NE norepinephrine neurons in the locus coeruleus LC show high activity during wakefulness low activity during sleep and zero during REM sleep gt Activation of ACh neurons produces cortical desynchrony waking and REM gt Histamine and orexin in the hypothalamus also appear L to play roles in sleep amp arousal r I Orxein stimulates appetite j I Lack of orexin can result in narcolepsy W J uncontrolled sleep J g Tamis p I I Losing all control of muscles and collapsing A dLsin quot eralple pu9 NOT fainting quot gt GABA is a major target for sedatives low levels of amil39aw GABA for arousal I I Neural control of SWS Basalforebrai gt sleep as an active process area gt ventrolateral preoptic area leOA in the basal Preoptic area forebrain is important for the control of sleep I Lesions of this area can cause total insomnia can lead to death in animals Magnocellular nucleus I Electrical stimulation of the leOA causes drowsiness I These neurons are MOST active in SWS I When leOA is on it inhibits arousal areas and inhibitory NE amp 5HT inputs ot leOA I Adenosine NT levels build up w sleep deprivation and adenosine injected into leOA of animals induces sleep onset I Caffeine does not stimulate but is an adenosine antagonist O Caffeine inhibits the body s water balance instead energy drinks gt Overall caffeine overdose causes anxiety insomnia tremors I Neural control of REM sleep gt The dorsal pons is important for the control REM seep gt PGO wavers are the 1st predictor of REM sleep gt ACh neurons in the pons modulate REM sleep I Increased Ach increases REM sleep I pontine neurons fire at a high rate during REM sleep I pontine lesions reduce REM sleep gt Pontine Ach neurons project to the reticular formation control of cortical arousal and to the superior colliculi REM gt Pontine cells project to the magnocellular neurons of the medulla which then inhibit spinal motoneurons induce REM motor inhibition Locus coeruleus Common Sleep Disorders gt Insomnia refers to a difficulty in getting to sleep or remaining asleep I Sleep Apnea person stops breathing as COz level rises and the brain kicks in forces them to breathing I Sometimes can awake them gt Narcolepsy sleep appears at odd times I Sleep attack I Cataplexy REM paralysis occurs person is still conscious I Sleep paralysis REM paralysis that occurs just before or just after sleeping 7 7 I REM sleep behavior disorder REM does NOT inhibit their body movements REM WITHOUT atonia I Sleep walking somnambulism during SWS I Fatal familial insomnia later in life suddenly develops insomnia and usually death occurs BIOLOGICAL RHYTHMS many of our behaviors and physiological systems display rhythmic variation 7 i I SWSREM cycles last about 90 min Elm I Circadian rhythms about a day 24 hrs 221 p232 sz iii d S a lll at iai yfi i 39p39e gt Light is an external cue zeitgeber that can set 5 Before the circadian rhythm L i 3 s Wk Over a long period of time subjects in the bunker were getting upatia b39out the time vexperimenterszoutsldethe bunker were going to bed gt In bunker Days 1015 The SCN in mammals Coronal sections through the anterior hypothalamus in a squir rel monkey Ieft rhesus monkey center and human right showing the location of the SCN 20 bilateral to the third ventricle Ill and dorsal to the optic chiasm CHO in all three species PA paraventricular nuclei 80 supraoptic nuclei Courtesy of Ralph Lydic k After bunker unnremlm Suprechiasmatic Nucleus SCN is a biological clock 0 gt Receives a direct projection from the optic H 39 fday tract It contains neurons that in the absence of a zeitgeber have a 25 hrs rhythms the blind tend to run on 25hrs rhythms until they match it W the human standard of time I Damage to SCN disrupt circadian rhythms gt Intact normal circadian patterns of activity in a nocturnal rodent W an intact SCN gt Following bilateral damage to the SCN the circadian rhythmicity is disrupted also disrupts REM rhythm of sleep 0 12 24 l Intact h 0 0 Dr SCNX Mu circadian W cm W 9Q h i i 39 a 3 I l r 39 I 5 l i I ll 5 3 LECTURE 12NEUROENDOCRINOLOGY sex 3 1 EE 3 35 1 hormones and the brain 39 39 39 39 5 Sexual determination and differentiation begins at fertilization 7 11 12 I Chromosomal XX or XY 23rd chromosome pair is P 3 z r5 5 53 5 determined at fertilization n u 15 I In people there are 46 chromosome in ALL our cells 1 W 1 except for spermatocytes and oocytes 33 3 r 39 v H1 b SEX CHROSOMOSOMES Chromosomal makeup decided 21 2 x Y which gonads develop and the gonads determine whether additional male or female characteristics develop I Sex determination vary for diff organism gt XXXO sex determination grasshoppers I Females are XX males are XO 39 Devempi39 head m W 39 gt ZZZW sex determination birds and amphibians j x I Males are 22 homogametic Females are ZW heterogametic I Developing heart gt Haplodiploidy bees wasps ants Sex based on of chromosome i Developing W sets in nucleus quot I Males haploid n femals diploid 2n quotFetal gonad I Environmental sexdetermination gt Temperature during embryonic development snakes and lizards v 1quot Genital tubercle gt Position in group mollusk s position in a stack of limpets f Chromosomal sex determine gonadal sex quotDevellilg leg I Generally female characteristics develop unless the system is instructed otherwise gt masculinization the induction of male characteristics gt defeminization the inhibition of female characteristics SRYsexdetermining region required codes for testis determining factor regions at the tips of the Y chromosome gt SRY cause maleness to be expressed I between the 6th and 7th week if there is XY develops into testicles Gonadal sex determines hormonal sex I if testes develop they begin to secrete hormones don t make sperm until puberty gt ANDROGENS ex testosterone is the result of testicular formation NOT the cause gt anti Mullerian horomone AMH peptide hormone inhibits the development of Mullerian ducts in the male embryo I If testes do NOT develop no gonadal hormone production for several weeks The ovaries do not begin to develop from the primordial gonad in human fetuses until about 12 weeks Internal reproductive tracts determined by hormones I Wolffian ducts vs Mullerian ducts organization effects and critical period gt Mullerian system gt Fallopian tubes uterus inner 23 of vagina I Absence of tests Mullerian develops gt Wolf an system gt epididymis vas deferens seminal vesicles I ONLY if stimulated by androgens AntiMUlleriaHormone I5 96 391 Gonad Epididymis Mesoneohros TESIIS Ovary M llerian duct quot Oviduct Vas deferens Wolffian duct Seminal vesicle I i I I i f Vii 39 Vagina a Prostate EALquot 333 Indifferent stage Female Male Hormones also determines external genitalia ANDROGENS determine which direction we go in for the internal reproductive tract we have two independent systems something masculiniz Testisdetermining factor 93 develop into testes STEPS in SEXUAL DIFFERENTIATION for the genitalia we can develop male or fea or in between LESS ANDROGEN LESS genital ation AntiMUllerian hormone Miillerian system withers away Defeminization Androgens Masculinization Androgens What can go wrong gt Complete androgen insensitivity an androgen receptor defect feminization at puberty m Pmtcm hormone action O 39H 7 33916quot g0 l39sm lost 0 ng l u l Altered 1 cell function biological gt Multiple effects h Steroid hormone action New protein production and multiple biological effects l and behavior In uence of androgens absence Of androgens 1 primarily dihydrotestosterone V M and V quot I out i 7 mar r m new 0 W immanen quot Testes descend into scrotum by 8quot month of human pregnancy l I r lean develops into fimbriae quot fallopian tubes uterus inner vagina 5am develo into ovaries No hormones Masculinization doesn t proceed very well Testes but no internal reproductive tracts female external genitalia further Biological sex Pseudohermaphrodite intersex Genetic sex xx ye xv Gonadal sex gm Y determined testes gs ovaries Hormonal sex testes determined androgens 8 AntiMiillerian hormone Ms no gonadal hormones Internal Reproductive Tract hormonally determined woman ducts ducts androgen stimulated and MIH inhibited or not External Genitalia DHT determined penis amp scrotum vs vulva The processes of sexual differentiation can affect sexual anatomy What about the brain In many sexual differentiation in uences physiology and sex differences in behavior an Sex difference in physiology some control Neurons synthesizing posterior pituitary hormones HYPOTHALAMUS components of male and female endocrine systems are different OVERVIEW of MALE NUEROENDOCRINOLOGY Some of testosterone s effects on the brain require its conversion to estradiol or DHT Neurons syntheslzlng at trophic hormones release 39 I V quot f 0 them into capillaries ol the portal system Artery Anterior pituitary adenohypophysis glandular pituitary vs posterior pituitary neurohypophysis neural pituitary gt Posterior pituitary grows from the diencephalon gt Anterior pituitary develops from the roof of the mouth no neurons at all Hormonal control of the anterior pituitary by the hypothalamus gt Hypothalamic neurons produce releasing amp inhibiting hormones which control synthesis and release of specific anterior pituitary hormones GnRH gonadotropic hormones controls FSH and LH Portal vessels carry the trophic hormones directly to the anterior pituitary Endocrine cells release their hormones into the second set of capillaries tor dlstrlbution to the rest of the body Terminals of hypothalamic neurons POSTERIOR PITUITARY P ANTERIOR PITUITARY Copynghl O ZUUI Pearson Euucalronr Inc Duelsmng as 80narnn Cummngs Fig 716 Where are these effects being exerted Sexuality Median I Hypophyseal eminence artery BRAIN me as hypothalamus She r d Primary plexus m GnRH Hypophyseal portal veins PITUITARY LH and FSH Secondary plexus W Posterior pituitary TESTES androgen spermatogenesis Cells that production Misfit produce anterior pituitary 0 mm 39 hormones 0 O Testosterone 9 E Anterior pituitary hormones Prolactin gonadotropic hormones FSH on and LH thyrord shmulatmg hormone GENITALIA ACTH growth hormone and REPRODUCTIVE SYSTEM on L 1 0 VI I J I 39 39 an a 3 a rm A A I14fo 5 393 5quot M Negative feedback at Arbuate nucleus gt Kisspeptin neurons in the arcuate are inhibited by high levels of gonadal steroids which then stop stimulating GnRH release at the 3921
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