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PSYC 220 EXAM 1 Study Guide

by: Lynde Wangler

PSYC 220 EXAM 1 Study Guide PSYC 220

Lynde Wangler
GPA 3.836

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All lecture notes as well as embedded study guide provided by instructor.
Meghan Jones
Study Guide
Biological Psychology
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This 21 page Study Guide was uploaded by Lynde Wangler on Sunday February 7, 2016. The Study Guide belongs to PSYC 220 at University of North Carolina - Chapel Hill taught by Meghan Jones in Spring 2016. Since its upload, it has received 103 views. For similar materials see Biopsychology in Psychlogy at University of North Carolina - Chapel Hill.


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Date Created: 02/07/16
PSYC 220 EXAM 1 COMPREHENSIVE STUDY GUIDE Week 1  Neuron parts: dendrites, axon terminal, myelin sheath, axon, soma (cell body), nucleus  Structure of Vertebrate Nervous System How is the nervous system divided and what functions is each division associated with? o Central Nervous System (CNS): consists of brain & spinal cord o Peripheral Nervous System (PNS): consists of afferent sensory neurons and efferent motor neurons; facilitate communication between CNS and the rest of the body  Somatic Nervous System: axons carry information from sensory organs to the CNS and from the CNS to the muscles  Autonomic Nervous System: controls innate/unconscious bodily functions; i.e., breathing, digestion, heartbeat, etc.  Terminology: o Dorsal(“back” – for humans closer to brain)/Ventral(“belly” – for humans downward or lower) o Anterior(front)/Posterior(back) o Rostral(towards the head)/Caudal(towards the tail) o Planes for Viewing the Brain: Horizontal(side to side), Sagittal(front to back), Coronal(top to bottom)  Spinal Cord: (Bell-Magendie Law) What is the difference between sensory and motor nerves? Where are their cell bodies located in relation to the spinal cord? o Dorsal root ganglia (collection of sensory neuron cell bodies coming into the spinal cord): Carry sensory information to the CNS o Ventral roots: carry motor information to innervate muscles; motor neurons have cell bodies within the gray matter of the spinal cord Where/what is white matter/gray matter? What is each composed of? How is it different in the brain and spinal cord? o Gray matter: center of spinal cord, densely packed cell bodies and dendrites o White matter: outer edge of spinal cord, mostly myelinated axons that carry information from gray matter to the brain and other parts of the spinal cord What is afferent vs. efferent? ***The dorsal roots carry sensory (afferent) information to the brain, while the ventral roots carry motor (efferent) information to command muscle movements. SAME – sensory, afferent, motor, efferent.  Peripheral Nervous System (PNS): o Autonomic Nervous System (ANS): controls “automatic” bodily functions by commanding heart, lungs, intestines, and other organs o Divided into Sympathetic and Parasympathetic Nervous Systems:  Sympathetic Nervous System:  “fight or flight”  Prepares body for activity by increasing blood pressure & heart rate and slowing digestion  Communicates primarily via neurotransmitter norepinephrine (primary neurotransmitter used by the Sympathetic NS)  Parasympathetic Nervous System:  “rest and digest”  Regulates activities including sexual arousal, salivation, urination, & digestion  Communicates primarily via neurotransmitter acetylcholine (primary neurotransmitter used by the Parasympathetic NS)  The Vertebrate Brain: Major Divisions of the Brain (better get on this because it is a LOT of information to know!!!) o Forebrain: Prosencephalon (“forward-brain”), Diencephalon (“between- brain”), & Telencephalon (“end-brain”) o Midbrain: Mesencephalon (“middle-brain”) o Hindbrain: Rhombencephalon (“parallelogram- brain”)  Structures of Fore-, Mid-, and Hindbrain: o Forebrain: thalamus, hypothalamus, cerebral cortex, hippocampus, basal ganglia o Midbrain: tectum, tegmentum, superior colliculus, inferior colliculus, substantia nigra o Hindbrain: medulla, pons, cerebellum  Hindbrain: o Medulla:  Extension of spinal cord; controls vital bodily functions (breathing, heart rate, coughing/sneezing, salivating) o The Cranial Nerves (V-XII):  Allow medulla to control sensations and muscles movements of the head; many parasympathetic outputs o Pons:  Anterior and ventral; site of decussation (crossing over) of motor information – axons from each hemisphere of the brain cross to the contralateral side of the spinal cord  Cranial Nerves: MEMORIZE  I. Olfactory: smell  II. Optic: vision  III. Oculomotor: control of eye movements; pupil constriction  IV. Trochlear: control of eye movements  V. Trigeminal: skin sensations from most of the face; control of jaw muscles for chewing and swallowing  VI. Abducens: control of eye movements  VII. Facial: taste from the anterior 2/3 of the tongue; control of facial expressions; crying; salivation; and dilation of the head’s blood vessels  VIII. Statoacoustic: hearing; equilibrium  IX. Glossopharyngeal: taste and other sensations from posterior third of the tongue; control of swallowing, salivation, and throat movements during speech  X. Vagus : sensations from neck and thorax; control of throat, esophagus, and larynx parasympathetic nerves to stomach, intestines, and other organs  XI. Accessory: control of neck and shoulder movements  XII. Hypoglossal: control of muscles of the tongue  Hindbrain: o Reticular Formation  Descending: controls motor areas of spinal cord  Ascending: sends output to cerebral cortex  Affects arousal and attention o Raphe System:  Sends axons to forebrain; regulates attention/readiness (raphe nuclei origin of serotonergic system) o Cerebellum:  Important for movement, balance, and coordination; shifting attention from one stimuli to another  Many folds (gyri & sulci)  (size/proportion) highly conserved across species  Midbrain: o Tectum: roof of midbrain o Superior and inferior colliculus: structures important for processing sensory information; inferior colliculus: hearing & superior colliculus: vision o Tegmentum: contains nuclei for cranial nerves; part of reticular formation o Substantia nigra: critical for movement planning and control; lack of dopamine in this region associated with Parkinson’s and Huntington’s diseases  Forebrain: o Outermost constitutes the cerebral cortex which is highly involved in processing sensory information and controlling movement of contralateral side of the body o Thalamus: “gateway to the cortex;” all sensory information is relayed through this region with the exception of olfaction o Pituitary gland: releases hormones into the blood stream (signaled by the hypothalamus) o Basal ganglia: caudate nucleus, putamen, and globus pallidus – critical for attention, planned movements, and learning (muscle memory) o Nucleus basalis (basal forebrain): critical for arousal, wakefulness, and attention  The Limbic System o Surrounds the brainstem; consists of several structures (olfactory bulb, hypothalamus, hippocampus, amygdala, cingulate gyrus) o Limbic structures are associated with emotion and regulate motivated behaviors (eating, drinking, sexual activity, anxiety, aggression, etc.)  The Cerebral Ventricles: CSF/Ventricles: Where does it come from? Where/How does it circulate? o Cerebral Spinal Fluid (CSF), produced in the choroid plexuses of the ventricles of the brain, protects the brain from harm by absorbing the impact should the brain be jostled; provides hormones and nutrients to the brain and spinal cord; interconnected system divided (only by name) into regions – lateral ventricle, third ventricle, fourth ventricle, cerebral aqueduct, spinal canal Wednesday Lecture: Neuroanatomy and Research Methods  Cerebral Cortex: o Most prominent in mammals; utilized for higher brain functioning and information integration o Divided into two hemispheres connected by anterior commissure and corpus callosum o Differences in size and folding between animals; more folds = greater surface area  Organization of the Cerebral Cortex: six layers are divided into perpendicular columns; divisions are based on functions  I. Molecular Layer – mostly dendrites and long axons  II. External Granular Layer – small pyramidal cells  III. Pyramidal Cell Layer – pyramidal cells  IV. Internal Granular Layer – small cells; main site for incoming sensory information  V. Inner Pyramidal Layer – large pyramidal cells; main source of motor output  VI. (a., b.) Multiform Layer – spindle cells  Human Cerebral Cortex: o Gyrus: ridges on cortex; hills; pl. gyri o Sulcus: groove on cortex; valley; pl. sulci o Four Lobes: Frontal (planning of movements, recent memory, aspects of emotion), Parietal (body sensations), Temporal (hearing and advanced visual processing), and Occipital (vision) o Precentral gyrus (primary motor cortex); Central Sulcus (divides Frontal and Parietal lobes); Postcentral gyrus (primary somatosensory cortex) Anatomy and Function of the Four Lobes of the Brain  Occipital Lobe: striate cortex/ primary visual cortex; heavily involved in visual processing; cortical blindness – people with this affliction have impaired visual cortices but intact visual structures so they can sense and detect visual stimuli to an extent but cannot perceive it; when asked to move out of the way when a ball is thrown at them, they are able to complete the task; also activated by visual imagery  Parietal Lobe: postcentral gyrus (primary somatosensory cortex); spatial information; integration of information from eyes and head; contains cortical map of the body (homunculus – explains foot fetishes)  Temporal Lobe: contains primary auditory cortex; language processing/production; damage can cause Kluver-Bucy Syndrome, which turns people into assholes – most common symptoms in humans include hyper orality, dietary changes, apathy or placidity, and may also cause agnosia and/or other memory disorders  Frontal Lobe: precentral gyrus (primary motor cortex); prolific dendritic branching to facilitate integration of information; Phineas Gage – railway construction worker who had a pipe blasted through his frontal lobe causing severe damage and ultimately a changed personality  negative effects (he became an asshole)  Prefrontal Lobotomy: removal of parts of the brain that connect prefrontal cortex to the remainder of the brain; used as a treatment for seizures and schizophrenia with very poor results  The Binding Problem o How do visual, auditory, and other parts of the brain operate to form a single perception of an object?  Maybe: the brain binds activities in areas when there is synchronous waves of neuron activity; “neurons that fire together, wire together”  For binding to occur, a person must perceive two sensations happening at the same time and same place (more information and examples in the book) Tools researchers can use to study the brain: what type of information do they provide (better spatial or better temporal resolution)? Which are invasive? What are the problems or difficulties associated with using each of the various methods?  Brain Research Methods:  Examine the effects of brain damage  Examine the effects of stimulating a brain region  Record brain activity  Examine the relationship between neuroanatomy and human behavior  Brain Damage: o Natural damage – damage or impairment might occur as result of an accident; not always reliable as much of the time, many areas are damaged simultaneously and so it is hard to study the effects of one not in conjunction with the other o Ablation: surgical removal of parts of the brain (archaic/crude method) o Lesions: destroying neurons in a specific area to study the effects – there are now much more sophisticated ways of suppressing activity in very specific neurons (stimulation, GABA, optogenetics, etc.) o Transcranial Magnetic Stimulation (TMS) – application of strong magnetic field to portion of scalp to suppress neuronal activity below the magnet; important to include controls (study active vs. inactive minds)  Gene Knock-out Approach: biochemical in nature; manipulates a gene of interest; can inactivate certain neurotransmitters or neuropeptide systems for a given phenotype or behavior  Brain Stimulation: o Electrical Stimulation – activates neurons in targeted region o Optogenetics – insertion of a light-activated proteins called opsin (can be achieved with an injection of a virus) to activate or silence particular neurons in the brain with a beam of light (laser will either depolarize or hyperpolarize the cells) o DREADD (Designer Receptors Exclusively Activated by Designer Drugs) – gene manipulation is used to express muscarinic receptors (which would normally be activated by Acetylcholine) that are now activated by Clozapine-N-Oxide; not as specifically localized as optogenetics but can use G-proteins to hyperpolarize and depolarize a neuron (to activate or inhibit an action potential); slower but longer lasting effects  Computerized Axial Tomography (CAT/CT Scan): o injects dye into the blood to increase imaging contrast; x-rays are passed through the head while the scanner rotates; used to diagnose/detect tumors, strokes, and atrophy in the brain provides structural information  Recording Brain Activity: o Electroencephalograph (EEG) – measures neuronal electrical activity in the brain; displays average activity of a given population of cells; used to measure activity during a task (controls are necessary) o Magnetoencephalograph (MEG) – uses magnetic fields to measure neuronal activity; better temporal resolution than EEG; when used during a task, requires necessary controls  Magnetic Resonance Imaging (MRI): o Hydrogen atoms exposed to magnetic field will align with said field; brief pulse of radio frequency applied; atoms will release energy as they return to their original positions; complex computer systems analyze the energy released and use it to map the structures of the brain and transform it into an image  Recording Brain Activity: o PET (Positron-Emission Tomography) – creates an image of the most active brain regions; uses radioactive tracer to measure activity; detects collision of positron and electron (from the decaying radioactive tracer, usually glucose) and measures the radiation that is emitted; high radioactivity means higher blood flow, which indicates greater activity; risk because of exposure to radioactivity but can look at specific neurotransmitters o fMRI (functional MRI) – uses BOLD(blood oxygen level dependent) signal (deoxygenated hemoglobin) to measure brain activity; better temporal resolution; oxygenated and de-oxygenated blood react differently to the magnetic field; often used when subject is performing tasks in the scanner; measures areas of activity by locating regions with deoxygenated blood  Relationship of Brain Mass to Body Mass Across Species: not very reliable  Cortical Areas Whose Size Correlate With IQ: (.3) weak relationship between size of brain and IQ; certain brain regions do correlate with IQ; neither measure of IQ nor measures of cortical area mass are reliable enough at this point to produce significant experimental results Friday Lecture: Nerve Cells and Impulses  Neurons: communication cells; humans have approximately 100 billion  Santiago Ramon y Cajal: Father of Neuroscience; created detailed and complex drawings that were mostly accurate; discovered that neurons are not connected to one another; Neuronal Doctrine – neurons are the smallest functional unit of the nervous system  Camillo Golgi – thought that neurons were connected (wrong); invented Golgi stain that uses silver chromate solution to stain individual neuronal cell bodies  Cell Structure: o Plasma Membrane – phospholipid bilayer; selectively permeable; serves as a barrier between outside environment and inside of the cell o Nucleus – located in soma; contains DNA o Mitochondria – energy source for the cell’s activities; powerhouse of the cell o Ribosomes – molecules than synthesize proteins in the cell o Endoplasmic Reticulum – structure that houses many ribosomes  Cellular Membrane: phospholipid bilayer (hydrophobic lipid tails and hydrophilic phosphate heads); have embedded protein channels (some voltage-gated) that either allow or do not allow certain molecules into the cell  Neuronal Structure: Neuronal Anatomy: what are the main structures in a neuron and what do they do? o Neurons have many of the same organelles as other cells but have distinct structures o Muscles and sensory organs are reached by long axons o Components of the neuron include soma, axon (with terminal), and dendrites  Dendrites: receive incoming cell signals; branching may be more or less extensive – the more branching there is, the more information can be received (more surface area for incoming “message”)  Dendritic Spines in Disorders: the number and condition of dendritic spines can be indicative of pathology in the brain – some diseases associated with abnormal spines are ASD (autism spectrum disorders), schizophrenia, and Alzheimer’s disease  Soma: contains the nucleus (and, accordingly, the cell’s DNA); determines cell differentiation; also contains other organelles such as mitochondria and ribosomes; densely packed site for synapses  Axons: Why Myelin Matters o Structure for carrying/transmitting messages from soma to other neurons o Myelin sheath covering speeds propagation down an axon; Nodes of Ranvier are breaks in the myelin sheath where ions can reenergize the action potential o Ex. A fibers carry pain information very quickly because they have myelination all along the fiber (initial pain felt), whereas C fibers transmit pain information more slowly and are less myelinated (aching pain felt – a reminder to the body to rest and recover) o Presynaptic terminals on the ends of axons release neurotransmitters that influence postsynaptic cells  Motor Neuron vs. Sensory Neuron: o Sensory Neuron (afferent) – dendrites are sensitive to incoming sensory information; transmit information along axon to the spinal cord o Motor Neuron (efferent) – cell body is in the spinal cord; sends information along axon to innervate muscles  Afferent vs. Efferent: think SAME (Sensory Afferent Motor Efferent)  The Diverse Shape of Neurons: neurons can be many different shapes and have different numbers of neurites and different amounts of branching; structure correlates with function; ex. Purkinje cell versus bipolar cell – more branching (in the Purkinje cell) means less acuity but it other cells (bipolar cells in the retina) there are fewer dendritic branches resulting in a more specific message o Bipolar Neurons – two neurites: one axon and one dendrite branching away from the soma (connector cell in retina) o Unipolar Neurons – some is attached to one neuron with one end branching to receive information o Multipolar Neurons – one axon with many dendrites branching off of the soma Glia: types, functions, microglia, oligodendrocytes, Schwann cells, radial glia and astrocytes  Glia: o Astrocytes:  Immune system of the brain; use cytokines (proteins), which can affect emotions; take up ions from the synapse and can release other molecules; remove waste materials when neurons die; “glue” ( really much more than that)  Also involved in memory, learning, and regulation of stress and emotions  Synchronizes the nervous system – tripartite synapse: glutamate regulation, gliotransmission, and calcium transients o Microglia:  Main immune defense for the nervous system; phagocytes – gobble up waste and dead neurons  Play a critical part in restructuring the brain with experience; neuroplasticity; “neurons that fire together wire together;” neurons not used may die and be consumed by microglia  Early in development, many synapses are restructured by microglia as our brain builds more efficient neural circuits (removes weak synapses)  Nervous system trauma incites immediate response from microglia (pro-inflammatory cytokines are released in abundance)  Oligodendrocytes and Schwann Cells: cells that compose the myelin sheath around axons; oligodendroglia are only found in the CNS, whereas Schwann cells are in the PNS only; nourish cell Myelin differences CNS and PNS  Radial Glia: guide migration of neurons; most eventually differentiate into neurons but others become astrocytes and oligodendrocytes  Fun Fact: Neurogenesis only occurs (as far as we know) in two regions of the brain – the olfactory bulb and an area of the dorsal hippocampus  Neurons vs. Glia: neurons have axons and glia do not; neurons house synaptic vesicles and communicate at the synapse and glia possess neither of the features; glia have the ability to divide (in response to injury, for example), whereas neurons do not Blood Brain Barrier: Function & Importance  Blood-Brain Barrier: filtering mechanism of blood vessels that carry blood to brain and spinal cord o Why do we need a blood-brain barrier???  In much of the body, our immune systems fight pathogens by killing off infected cells… neurons do not regenerate readily, so this is NOT a viable option in the nervous system hence, we have a barrier to keep out unwanted viruses, molecules, other substances, etc.  Microglia do have the ability to lead an immune response without killing neurons but it is often not completely effective (ex. chicken pox shingles) o What can get through the blood-brain barrier???  Small uncharged particles can get through (oxygen and carbon dioxide); any molecules that are fat-soluble and will dissolve in the membrane (this includes vitamins and drugs that act on the brain); active transport (requires energy so that a protein embedded in the membrane can transport a molecule across) allows useful chemicals such as glucose, amino acids, and hormones to cross o Why do we sometimes get annoyed with the blood-brain barrier???  It prevents molecules getting through that might be helpful in solving problems in the brain – for example, this is why brain cancer is so difficult to treat  Nourishment of Vertebrate Neurons: o Glucose and Oxygen – readily available/accessible (more so than ketones or lactate); made with amino acids and carbohydrates; PET – glucose, fMRI – deoxygenated hemoglobin o Thiamine and Vitamin B (prerequisite to using glucose) – Korsakoff’s syndrome: neuronal death  memory impairment  The Nerve Impulse: neurons are responsible for transmitting information to all the remote regions of the body and often over long distances; message (action potential) is regenerated along the axon and does not decay as it is propagated to the axon terminal  Balancing Electrochemical Forces: living cells possess electrical charges; anions are negative and cations are positive; vocab to know: ions, cations, anions, intracellular/extracellular fluid important for discussion of action potentials (neuron communication)  Resting Membrane Potential: o Electrical Gradient (or Polarization) – the difference in charge across a membrane; the difference in electrical charge of the inside of the cell versus the outside environment o Voltage-gated ion channels in the semi-permeable cell membrane determine the state of the cell…(more to come) WEEK 2 Concentration and Electrical Gradients: how are these involved with movement of ions?  Electrical versus Chemical Signaling: o Electrical: an action potential is propagated down an axon via salutatory conduction (of an electrical signal); electrical signal can travel anywhere from 1m/s to 100m/s o Chemical: communication between neurons occurs via chemical signaling (using ions and neurotransmitters)  Membrane Potential Review – polarization (aka electrical gradient) is the difference in charge across the membrane (difference between inside and outside charges of a cell); membrane potential change is dependent upon ion movement o Diffusion: passive transport of ions from a high concentration to a low concentration o Electrostatic Pressure: refers to the quality of ions that causes ions of opposite charges to attract and those with like charges to repel one another  For ex., because potassium is more concentrated within a cell at resting potential, the concentration gradient will want to push K+ out of the cell. However, electrostatic forces dictate that since the inside of the cell is more negative, K+ will come into the cell  at resting membrane potential the K+ is approx. at equilibrium (that is, there is no net flow of this ion  Recording Membrane Potential – place one electrode in a solution outside the cell and the other inside the cell; the number recorded in the difference in millivolts between the two o Resting Potential – (for humans) ~-70mV but different people and different neurons vary (ranges from about -60mV to -80mV)  Selectively Permeable Cell Membrane: How does permeability affect the movement of ions? o Voltage-Gated Ion Channels: open and close in response to electrostatic changes across the membrane  Potassium, Sodium, Chloride, Calcium o Resting Membrane Potential: approx. -70mV; refers to state of neuron membrane before an electrical signal (action potential) is sent  Methods for Recording Activity of a Neuron: place electrodes in and around neuron to measure electrical differences; i.e., occurrence of action potentials can be observed  Sodium-Potassium Pump: What is the role of the sodium-potassium pump in an action potential?  Exchanges internal Na+(3) for external K+(2)  Maintains electrochemical gradient to maintain resting potential  Does NOT cause large changes in membrane potential; works in the background  Equilibrium Potential  ions at resting potential: Distribution of Ions at Rest o Inside the Cell – many K+ ions and Proteins with negative(-) charges o Outside the Cell – many Na+, Ca2+, and Cl- ions  Movement and Forces on Ions: o Sodium is pushed into the cell both by concentration gradient and electrical gradient o The concentration gradient would like to push K+ out of the cell so if the K+ channels were wide open (as they are during the falling phase of an action potential) K+ would flow out o Leaky potassium channels – not voltage-gated; allow a small number of K+ ions to exit the cell at resting potential while the Na+ channels are closed  Action Potential Sequence of Events:  How is the strength of the stimulus reflected by the action potential? – not by the magnitude (all action potentials will have similar magnitude once threshold of excitation has been reached) but by frequency of firing o Action potentials originate at the axon hillock (the region on the soma right before the axon begins) strong changes in membrane potential are propagated down the axon regeneration at each node of Ranvier ensures that the signal does not decay the electrical signal communicates to the cell information about how to communicate with the next cell via processes in the axon terminal (coming soon) o Steps: Molecular Basis of the Action Potential  1) Resting Potential – K+ equilibrium, sodium channels are closed, leaky potassium channels are open  2) Depolarization – voltage-gated sodium channels open up allowing Na+ to flood into the cell depolarizing (making the inside of the cell less negative in comparison to the outside) the neuron  3) Reversal of Potential – occurs when the electrostatic potential exceeds 0; the inside of the cell is now positive relative to the outside; called the “overshoot” and this is when Na+ is almost at equilibrium Why does an action potential not travel backwards? (hint: types of refractory periods) see stages 4 & 5  4) At (shortly after this point) sodium channels are INACTIVATED (absolute refractory period – they cannot open so an action potential CANNOT be generated) they then close; K+ flows in excess out of the cells with the concentration gradient and the charge then becomes more negative again Why is the action potential hyperpolarized briefly, before the membrane potential returns to resting values?  5) K+ ions continue to flow out causing hyperpolarization of the cell (relative refractory period); aka undershoot; occurs before returning to resting membrane potential when K+ channels close, which is maintained by the sodium-potassium pump Hyperpolarization vs. Depolarization  Hyperpolarization – membrane potential moves away from zero; becomes more negative; -80mV; difference between inside and outside of the cell is greater  Depolarization – less difference between inside and outside of cell; membrane potential is closer to zero more positive (but less than zero)  Threshold of Excitation: subthreshold stimulation creates a response that then quickly decays; an action potential occurs only when the stimulation is strong enough to reach threshold of excitation  Reversal Potential/ Reversed Polarity – the peak of the action potential reaches a positive number above zero; the inside of the cell is now positive relative to the outside of the cell  Blocking Action Potential: o Scorpion venom keeps sodium channels open and blocks potassium channels; toxic levels of sodium build up in the neuron  The All-Or-None Law:  Amplitude and velocity of action potential are not dependent on the strength of the stimulus; If threshold of excitation is met, then an action potential will be generated stimulus intensity is coded by the frequency of firing  Action Potentials Travelling in Reverse: they can back-propagate into soma and dendrites (structural changes in dendrites are associated with learning); normally action potentials travel in only one direction toward the axon terminal because of the absolute refractory period where the previously open sodium channels are inactive  Propagation of an Action Potential: saltatory conduction the signal jumps and is regenerated down the axon at each node of Ranvier; speed is influenced by diameter of axon (larger = faster) and degree of myelination Why does myelin matter and how does it affect transmission of an action potential?  Demyelination Disorders: o Multiple sclerosis – muscle weakness; impaired motor function; impaired speech, vision, and cognition; genetic and environmental causes o Guillain-Barre syndrome – autoimmune disease; muscle weakness starting in legs and travelling upward in time; environmental causes  Dysmyelination Disorders: o Tay-Sachs disease – progressive degeneration of motor and cognitive abilities; causes very young deaths (before age 4); genetic disease o Schizophrenia  Local Neurons and Graded Potentials: o Do not have axons; exchange information with neurons that are very close; produce graded potentials (vary in magnitude and can be inhibitory or excitatory) depolarizes (excitatory)/hyperpolarizes (inhibitory) o Myth – only 10% of neurons are active at any given time……(UHM NOOO) WEEK 3  Molecular Basis of the Action Potential:  Resting membrane potential (-70mV); maintained by sodium- potassium pump; more internal potassium and external sodium  Leaky potassium channels are open and some sodium channels are open allowing the membrane to depolarize slightly  BUT THEN  The threshold of excitation is reached and the neuron depolarizes when voltage-gated sodium channels allow sodium to flood into the cell  Membrane potential continues to rise and reaches reversal of potential (overshoot) when the relative charge of the inside is more positive than the outside  At this point voltage-gated potassium channels open and K+ floods out into the extracellular space repolarizing the cell; also at this point sodium channels are DEACTIVATED (not closed)resulting in absolute refractory period  K+ continues to leave the neuron resulting in an undershoot and sodium channels reset (relative refractory period); another action potential can be generated but greater stimulation is required  Resting potential is restored  Manipulating Action Potentials: o Scorpion venom keeps sodium channels open; excess sodium is toxic o Local anesthetics block sodium channels preventing an action potential from occurring  Sodium-Potassium Pump: maintains resting membrane potential; exchanges internal sodium for external potassium (think salty banana – potassium in the cell and sodium in the extracellular fluid)  The All-or-None Law: the magnitude of the action potential is not dependent upon the strength of the stimulus; once the threshold of excitation has been met, an action potential will fire with an invariable magnitude that will not decay as it travels down the axon due to saltatory conduction when action potentials jump from node (of Ranvier) to node  Why Don’t Action Potentials Travel Backward? – voltage-gated sodium channels in the membrane where the cell has already been depolarized are inactivated for just long enough that there are no longer any sodium ions to (re)depolarized the neuron; absolute refractory period  Propagation of an Action Potential: thicker axon = faster conduction; myelination = faster conduction Lecture 1/29/16 Synapses  Myelin Sheath – increases membrane resistance (ions do not leak out across the membrane from the inside); decreases membrane capacitance; allows action potential to jump from node to node without losing magnitude  Synapses – chemical (as opposed to electrical) transmission was not widely accepted until the 1950s Charles Sherrington coined the term synapse in 1906: o Studied reflex arc-circuit (consists of sensory neuron, interneuron, and motor neuron); 3 observations:  Reflexes are slower than conduction along an axon (something was slowing the information to the muscles)  Weak, subthreshold stimuli could cause a reflex when combined together (EPSPs & IPSPs by temporal and/or spatial summation) Temporal vs. Spatial Summation – temporal summation is when a neuron is receiving impulses one after another in quick succession at the same point and spatial summation is when a neuron receives many messages at one time in different places on the dendrite  One set of muscles is excited while one is inhibited (studied dogs’ flexor and extensor muscles of the legs and found that when one flexed, the other three extended and the flexor muscles relaxed)  Characteristics of Electrical Signals of Nerve Cells EPSPs/IPSPs/Action Potential Differences Action Conduction Overshooting All-or-none First Na+ Voltage- Potential along axon then K+ gated channels EPSP Transmissio Depolarizing Graded Na+ K+ Chemically n between regulated neurons IPSP Transmissio Hyperpolarizi Graded K+ Cl- Chemically n between ng regulated neurons o EPSPs and IPSPs alter the spontaneous firing rate of neurons (neurons are always active) What was Loewi’s experiment and what did it prove existed?  Otto Loewi – proved that chemical communication occurs across synapses; stimulated the vagus nerve of a frog heart and then put a different heart in the solution that the first heart was in and observed the same effects cannot harness loose electricity so it must have been chemical  Steps of Synaptic Transmission:  1) Neurotransmitters are synthesized in the presynaptic cell and packaged in vesicles  2) Action potential causes Ca2+ to enter prompting exocytosis of the vesicles, releasing the neurotransmitters into the synaptic cleft  3) Neurotransmitter binds to receptor on postsynaptic cell causing a variety of effects (depending on the neurotransmitters and receptors)  4) Neurotransmitters release from receptors and is taken back to the presynaptic cell by transporter proteins  5) Postsynaptic cell releases retrograde transmitters signaling the presynaptic cell to limit release of further neurotransmitters  6) Negative feedback sites on presynaptic cell respond to retrograde transmitter  Neurotransmitters: chemicals that travel across the synapses to affect the postsynaptic cell o Amino Acids – glutamate (+), GABA (-), glycine(-), aspartate, etc.; modified amino acid  Ach (acetylcholine) o Monoamines – serotonin; dopamine, norepinephrine, epinephrine (catecholamines) o Neuropeptides – endorphins, substance P, neuropeptide Y, etc . o Purines – ATP, adenosine o Gases – NO (nitric oxide) NOT nitrous oxide (laughing gas)  Neurotransmitter Release: most neurotransmitters are synthesized in the synaptic terminal and are then stored in vesicles influx of calcium causes the vesicles to undergo exocytosis and release the neurotransmitters into the synaptic cleft o MAO inhibitors – monoamine oxidase breaks down transmitters into inactive chemicals  Activating the Postsynaptic Neuron: effect on postsynaptic cell depends on the neurotransmitter and that transmitter’s receptors; there are either ligand- gated or transmitter-gated channels o Ionotropic Receptors: neurotransmitter causes protein channel to change its shape and allow ions to flow in; faster but effects are short- lived; mostly rely on Glutamate (+) and GABA (-) o Metabotropic Receptors: initiate a sequence of metabolic reactions; slower but longer-lasting effects; acts through a second messenger (like cAMP) activated by a G-protein WEEK 4 2/1/16 Chapter 2 Synapses  Clarification: food does not directly cause neurotransmitter release – amino acids that come from you diet can influence the supply of different types of neurotransmitters  Ionotropic – fast, shorter-lasting effects, one effect, activated by smaller neurotransmitters  Metabotropic – slower, longer-lasting effects, can have many effects, activated by larger neuropeptides (through G-protein and secondary messengers)  Gap Junctions – at electrical synapses, very quick, direct flow of ions across a very small space between cells, needed in areas where synchrony is necessary (brain in early development has many of these junctions to synchronize growth and neural circuitry formation)  Features of Neuropeptides: Neuropeptides Other Neurotransmitters Synthesized in the cell body Synthesized in the pre-synaptic terminal Released from dendrites, cell body, and Released from axon terminal sides of axon Released by repeated depolarization Released by single action potential Diffuse to wide area Effect on receptors of adjacent post- synaptic cell Duration of effect: minutes Duration of effects: less than a second to a few seconds Types of Neurotransmitters and Where They Come From:  Acetylcholine (Ach) – chemical from Otto Loewi’s frog heart experiment (basis of proof for chemical communication between cells); diffuse modulatory system: cholinergic originates in basal forebrain; loss of cholinergic neurons is noted in individuals with Alzheimer’s disease, which suggests that this neurotransmitter is important for learning and memory  Dopamine (DA) – diffuse modulatory system: dopaminergic; 2 main pathways   Mesostriatal Pathway: origin is substantia nigra and projects to the striatum; DA important for movement and motor control (Parkinson’s patients have loss of dopamine producing cells)  Mesolimbocoritcal Pathway: origin is VTA (ventral tegmental area) and projects to the limbic system and cortex; abnormalities of this pathway are associated with schizophrenia and addiction; important for reward and motivation  Norepinephrine (NE): diffuse modulatory system: noradrenergic; important for mood, arousal, sexual behaviors; sympathetic fibers of the body use this transmitter; 2 main pathways –  Locus Coeruleus – in the pons  Lateral Tegmental Area – in the midbrain  Serotonin (5-HT): diffuse modulatory system: serotonergic; origin in the Raphe Nuclei; important for sleep, mood, anxiety, and sexual behavior; used in anti-depressants (SSRIs) How are neurotransmitters broken down/reused/recycled?  Neurotransmitter Reuptake: neurotransmitters will either be inactivated or taken back up and recycled; transporters are membrane proteins that collect neurotransmitters for reuse; COMT – enzymes that convert excess into inactive chemicals o Serotonin – taken back up into presynaptic terminal by transporter proteins o ACh – broken down by acetylcholinesterase into acetate and choline o Excess dopamine is converted into inactive chemicals  Negative Feedback from the Postsynaptic Cell: accomplished in one of two ways – o Autoreceptors – detect amount of transmitter released and inhibit further synthesis and release o Postsynaptic Neurons – respond to simulation and send retrograde transmitters to the presynaptic terminal where they inhibit further release (transporter proteins)  Neuropeptides: Neuropeptide Y – anxiogenic (anxiolytic = antagonist); Substance P – pain; Orexin – hunger  Hormones: chemicals secreted by endocrine glands and transported via the bloodstream to target organs where they alter activities; responsible for triggering long-lasting changes in multiple parts of the body (think puberty, for example); hypothalamus secretes releasing and inhibiting hormones that control different endocrine glands; endocrine glands can send inhibitory messages (negative feedback) to the hypothalamus to regulate hormone concentrations in the blood o Pituitary Gland (“The Master Gland”) – attached to hypothalamus; secretes releasing and inhibitory hormones that regulate anterior pituitary hormone production; synthesizes vasopressin and oxytocin which migrate to posterior pituitary o Anterior Pituitary:  Growth Hormone (GH) – body growth  Adrenocorticotropic hormone (ACTH) – increases steroid hormone production by the adrenal glands  Thyroid Stimulating Hormone (TSH) – stimulates thyroid gland  Follicle Stimulating Hormone (FSH) – promotes ovum maturation and sperm production for respective sexes  Luteinizing Hormone (LH) – stimulates ovulation  Prolactin – increases milk production o Posterior Pituitary: neural tissue, releases vasopressin and oxytocin (hormones synthesized in the hypothalamus)  Oxytocin – uterine contractions, milk release, sexual pleasure  Vasopressin – raises blood pressure, decreases urine volume o Adrenal Gland: part of HPA axis (hypothalamus-pituitary-adrenal axis); hypothalamus synthesizes and secretes CRH (corticotrophin releasing hormone) stimulates anterior pituitary to release ACTH  stimulates adrenal glands to release cortisol (in rodents called corticosterone); important in stress response mechanisms, sympathetic nervous system activation o Ovary: estrogens and progesterone  female sexual characteristics and pregnancy o Testis: testosterone male sexual characteristics o Kidney: Renin regulates blood pressure, contributes to hypovolemic thirst (thirst due to loss of blood volume)  Endogenous – substances that are made within an organism  Exogenous – substances that do not originate from within the body  Drug Effects o Agonist – binds to receptor site and activates receptor like an endogenous substance would o Antagonist – binds to the receptor either at the ligand binding site or another site and blocks activation of the receptor  Affinity vs. Efficacy o Affinity – the likelihood that a drug will bind with a receptor o Efficacy – the likelihood that the drug will activate the receptor o Different receptors have differing affinities for different ligands; a drug is classified as agonist or antagonist depending on the overall effect of the response  Ex. How would you classify a drug with high affinity but low efficacy? – in areas where receptors are open, the drug will increase activity and in areas where the endogenous substance is not lacking, the drug will decrease activity because it will act as a competitive agonist (this will decrease activity even if all the receptors are active because the drug is less effective than the endogenous molecule would be)  How Do Drugs Influence Synaptic Transmission? o Presynaptic Process: Neurotransmitter production and release, autoreceptors – limit neurotransmitter release from presynaptic terminal, neurotransmitter clearance – reuptake inhibitors o Postsynaptic Process: transmitter-receptor selective drugs (agonist or antagonist), downstream processes that regulate receptor expression or prevent cell’s ability to respond  Amphetamine & Cocaine – stimulate DA synapses; increase release of DA from presynaptic terminal  Methylphenidate (Ritalin) – blocks reuptake of DA at a gradual and more controlled rate; prescribed for people with ADD (we don’t know if use in childhood causes higher likelihood of drug abuse in adulthood)  Some drugs of abuse have their own receptor because they are chemically similar to endogenous compounds that the human body makes and uses  Cannabinoids – autoreceptors  Opioids – opioid receptors 2/3/16 Chapter 4 Genetics & Evolution  Is Development Shaped by Genetics or by the Environment? – Mendel (studying pee plants) was able to determine that inheritance occurs through genes, which are units of heredity with structural integrity  Disposition for developing psychological disorders, weight, personality traits, success, sexual orientation  What is DNA? (Basic Biology Review) o Gene – part of chromosome composed of DNA (deoxyribonucleic acid) o Chromosome – strands of DNA; exist in pairs (except XY) o Homozygous – identical pair of genes of each chromosome o Heterozygous – differing pair of genes on each of two chromosome  RNA: one strand of DNA; order of bases on an RNA molecule determines the order of amino acids which then code for certain proteins  regulatory functions; structure of body; enzymes that regulate chemical reaction throughout the body  Dominant vs. Recessive genes – Phenylthiocarbamide (PTC) is a dominant trait for supertasters; there are dominant, recessive, and intermediate genes  Sex-linked – gene is on X or Y chromosome (females: XX, males: XY); gene that controls color blindness is on the X chromosome males are more often color blind than females  Sex-limited – gene is present in both sexes but active in only one; sex hormones are responsible for activation of these genes  Genetic Changes: o Mutation – a heritable change in DNA (occurs through duplication or deletion)  Epigenetics – the concept that genes can be turned on or off by experience; ex. rat pups born to malnourished mother show increased propensity for obesity & rat pups with low degree of maternal care show more likelihood of developing emotional stress issues  How Is This Possible?? o Histones bind DNA and must be unbound from the DNA for it to be activated; epigenetic influences modify histone tails near a gene  Heredity: o Heritability – degree to which a trait being passed on depends on genetics o How do we study heritability? – twin studies, adoption studies, link gene to phenotype o Environmental modification – Phenylketonuria (PKU), alter diet and there are no problems  How Genes Affect Behavior – some genes control brain chemicals but other genes affect behaviors indirectly  Evolution of Behavior: any gene associated with higher reproductive success will be kept in the gene pool and in greater prevalence than other genes; Artificial Selection vs. Natural Selection no evidence for Lamarckian evolution (you don’t lose it if you don’t use it; he thought that physical characteristics such as strength could be passed directly from parent to offspring); fitness (“survival of the fittest”) is measured by one’s ability to pass on genes to the next generation  evolution benefits genes  Brain Evolution – nutrition hypothesis; more genes active during development; study with guppies  Evolutionary Psychology – study of natural selection with regards to genes that may promote certain favorable (for fitness) behaviors (ex. males have many more sexual partners than women because it takes ten minutes compared to nine months for women to pass on his/her genes)  Altruistic Behavior: o Actions that benefit someone other than the person committing the action o Hard to find examples in non-human species o Kin Selection – selection for a gene that benefits the individual’s relatives 2/5/16 Chapter 4 Development of the Brain  Brain Size – birth (350g), 1 year (1000g), and adult (1200-1400g)  Nearly all neurons form within the first 28 weeks of conception  Stages of Development: o Neurogenesis/Proliferation: cells lining the ventricles divide; either become primitive neurons or glia that migrate to other locations of remain as stem cells to continue dividing; neurogenesis in adulthood is limited to the olfactory bulb and part of dorsal hippocampus; Stem Cell Research has potential to aid Alzheimer’s and Parkinson’s diseases research o Cell Migration: chemical process guided by immunoglobulins and chemokines that guide neuronal migration; radial glia o Differentiation: axons, dendrites, and cell bodies vary in structure depending on the cell’s ultimate fate; axons grow first, during migration; dendrites and cell bodies form once the cell reaches its destination; final fate depends on what neighboring cells are doing – affects chemicals released, patterns of firing, etc. o Myelination: occurs first in spinal cord then hindbrain, midbrain, and forebrain; continues gradually throughout adolescence; vulnerable to problems introduced by experience (composed of oligodendrocytes & schwann cells) o Synaptogenesis: formation of synapses; begins before birth and continues throughout life o Neuronal Cell Death: o Synapse Rearrangement:  Chemical Pathfinding by Axons: Question – Do muscles that neurons attach to determine their function or do neurons already have a predetermined function and attach to very specific regions? –Paul Weiss, 1924: regenerated a salamander limb and because it was then able to move concluded that the muscle determines the neuron (WRONG) o Roger Sperry conducted an experiment in 1943 where he cut a newt’s optic nerve and rotated its eye, but the axons still grew back to their original targets  Chemoattraction – axons migrate to targets with a similar chemical gradient and then form synapses with many cells around the correct location  Neural Darwinism – each target cell receives synapses from many different axons and only those that are the strongest will survive – synaptic pruning is not random o How do the Right Number of Synapses Form?  Apoptosis – programmed cell death (all cells are programmed for death unless told otherwise) Nerve Growth Factor (NGF) promotes survival and activity of neurons (cancels apoptosis, periphery vs. brain)  Brain-Derived Neurotrophic Factor (BDNF) – another neurotrophin that promotes survival and synaptic strength (learning and depression)  Necrosis – unplanned cell death  Fetal Alcohol Syndrome: condition caused by prenatal alcohol consumption characterized by hyperactivity, impulsiveness, difficulty maintaining attention, mental retardation, motor problems, heart defects, and facial abnormalities slows proliferation, inappropriate migration and differentiation, decreased synaptic transmission (possible cortical cell death)  Differentiation of the Cortex – chemical gradients guide neuronal migration, but when do neurons differentiate exactly during development? – ferrets are born so immature that their optic nerve has not yet reached the thalamus  SO…scientist damaged superior colliculus and occipital cortex (optical target) and auditory input on same side, leaving the other side of the brain to function normally o Results: auditory thalamus and cortex reorganized; ferret responds to a visual stimulus as if it were an auditory stimulus  Fine-tuning By Experience: environmental enrichment (affects dendritic branching and overall functioning of neurons), exercise, sensory adaptations, and phantom limb  Brain Adaptations and Stroke (ischemia, hemorrhage, etc.) – coming soon (Monday lecture, be there or be 


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