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Course notes/Final review

by: Desiree Scinski

Course notes/Final review Psych 3

Desiree Scinski
Bio basis of psych

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About this Document

My personal notes for the course. Separated by topic.
Bio basis of psych
psych, Psychology, UCSB, psych 3, bio basis of psych, biopsych
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This 82 page Bundle was uploaded by Desiree Scinski on Tuesday September 22, 2015. The Bundle belongs to Psych 3 at University of California Santa Barbara taught by Barany in Summer 2015. Since its upload, it has received 11 views. For similar materials see Bio basis of psych in Psychlogy at University of California Santa Barbara.


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Date Created: 09/22/15
Neuroanatomy Tuesday August 4 2015 1237 PM Week 1 Tuesday The NS Divided into 2 parts 0 Central Nervous system 39 Brain Spinal cord is a single system 0 Peripheral nervous system Navigating the CNS AnteriorRostral towards the front PosteriorCaudal towards the back Dorsal up towards your back Ventral down towards yourabdomen When talking about these directions in terms ofthe spine you mustflip 90 degrees Superior up lnferior down Medial towards the midlinecenter Lateral away from the midlinecenter me side ofthe midline opposite sides of midline Ex The right arm is ipsilateral to the right hemishere and contralateral to the left hemisphere Proximal closer to the body Distal farther from the body Ex The hand is distal to the shoulder The shoulder is proximal to the hand Planes ways to divide the brain Horizontal splitting top half of body from bottom half through the middle of the body splitting nose through the middle ofthe body splitting frontfrom back Protection forthe CNS protect the brain 0 3 typeslPADl o Qura mater o Arachnoid 0 Bio mater No pain receptors in brain many in meninges Headaches often due to irritation of dura Aneurysm blood vessel rupture in subarachnoidspace Meningitis infection of meninges through bloodstream Meningioma tumorin meninges often very small and benign Protection forthe CNS 0 Cushioned for the brain Produced in the ventricular system Circulates through ventricles central canal of spinal cord and subarachnoid space Reabsorbed into bloodstream Hydrocephalus when CSFfowis blocked causes head to enlarge bc much more CSF in head Protection forthe CNS Protects the brain from some substances in blood 0 Stroke Disorder of blood vessels that often leads to breakdown ofBBB and damages certain brain regions Divisions ofthe CNS CNS early development 0 Brain develops 3 swellings o Forebrain 39 Telencephalon I Diencephalon o Midbrain 39 Mesencephalon o Hindbrain 39 Metencephalon I Myelencephalon 0 First sign of brain development Spinal cord ventral roots have only motor efferent neurons dorsal roots have only sensory afferent neurons 0 Specific segments of the spinal cord have to do with specific parts of the body A E l n M nn nn nF FHVquotI nnvnl 39FIIII nar l1rro DnInlnm nF FHVquotI nnvnl nnhl knInlnm U EX UCIIIICIBC LUPUI bpllldl LUIU IUII pdldlelb DULLUIIIUI bpllldl LUlU Ullly UULLUIII paralysis Myelencephalon medulla amp Metencephalon 0 Medulla pons and reticular formation regulates reflex activities critical for survival ex Heart rate respiration sleep arousal 0 Cerebellum quotlittle brainquot motor coordination and balance Mesencephalon midbrain 0 Superior colliculus head orientation eye movements 0 Inferior colliculus auditory relay 0 Substantia nigra sensorimotor 0 cells die in patients with Parkinson39s disease Diencephalon 0 Thalamus Relay site forsensory processes 0 Hypothalamus Involved in hunger thirst temperature regulation reproductive behavi0I and aggression 0 Pituitary Gland site of hormone secretion 0 Optic chiasm where the two optic nerves meet and cross Telencephalon Precenlral Central L ss malral gyms fussu39c 391 quotUs l alfnml Ilssulu Supunm lumpoml wruei 0 Fissu res Large grooves 0 Sulci Small grooves 0 Gyri Ridges Limbic System Hippocampus memory Occipital Lobe Visual processing Somatosensory processing spatial attentior Temporal Lobe Auditory processing memory object reco Motor control reasoning inhibitory control working memory Corpus callosum Tracts connecting the two hemispheres Y39S gnition Amygdala emotion Basal Ganglia motor control Cells ofthe NS Neurons Cell body y Dt ntl rllt S Neuronfundamentalfunctional unit ofthe nervous system specialized cells for the reception conduction and transmission of electrochemical signals Glia Nonneuronalcells variety offunctions o quotgliaquot means glue 86 billion neurons in the brain 1 billion neuronsin the spinal cord About the same number ofglial cells as neurons in the brain Cell body soma metabolic center Cell membrane encloses the neuron semipermeable Dendrite receives input Axon sends nerve impulses 5 Axon terminal the end of an axon forms a synapse with li p1 another neuron l iii Neurotransmitters molecules released from neurons across tr ll synapse Axon xl i Variety of neurons l Axon v Unipolar neuron Bipolar neuron 0 Multipolar neuron ll is Multipolar interneuron al ii 0 N 1 el 1 If v A 2 1 v gt Il l 1 x terminals 7 393 MR UC k r S39 VCNK KlNS V I w39lh minor Visualizing nerve cells Golgi stain Cant see inside Nissl stain can see clear structures of cell bodies but only cell bodies Brain bow neuron express different proteins in different colors Two types of neurons in neocortex o Pyramidal cells really long axon 80 of neurons o Stellate cells interneu rons so don t really have axons Gray matter cell bodies White matter myelinated axons 0 Connections between regions Glial Cells lVIyelin fatty tissue that speeds up neural conduction Oligodendrocytes form myelin sheaths around axons in CNS Schwann cells form myelin sheaths around axons in CNS Astrocytes starshaped cells that support and provide nourishmentfor neurons among other functions Microglia small cells that remove debris from injured or dead cells Glia are more than just quotgluequot Astrocytes communicate with each other and with neurons Defective glia plays a role in neurological diseases such as Alzheimer39s disease and Amyotrophic Lateral Sclerosis ALS Themes StructureFunction o The meninges protect the brain because their pain receptors help you to know when something is dangerous and stops you from brain damage 0 The 3 layers ofCNS the PAD the organization ofthe meninges protects the brain from hard things on outside and cushions it by being soft on inside 0 The way that CSF is organized inside the brain being the central structure allows ii to flow throughout all of brain 0 What does the structure ofthe neuron tell us about its function 39 The way neurons are organized NewResearch o Glia isntjust a glue 0 Brainbow Bio psych Intro Monday August 3 2015 1224 PM Week 1 Monday Scientific study of the biology of behavior 0 A discipline of neuroscience the scientific study of the nervous system Can the brain understand itself quotYou only use 10 ofour brainquotMYTH FALSE 0 The brain is 2 of our body weight and accounts for 20 of body39s total energy consumption 0 Only 1 ofthe brain39s energy usage deals with external inputs the outside world Themes 1 Structure and function ofthe nervous system are closely related a Structure anatomy Function processes 2 The nervous system adapts and changes itself over time a Learning something new Experience Ability of brain to reorganize itself after injury Nervous system is dynamic process that s always changing as it interacts with the world becoming more specialized and efficient 3 Our view ofthe nervous system is rapidly evolving a New methods being developed often History of bio psych How are the mind and body related 0 Older civilizations didn t care much for the brain more care for spinal cord Aristotle thought mind resided in heart brain just used to cool blood 3353C 1504 DaVinci said resided outside of body ventricles in brain had different spirits one for cognition one for memory etc o ChurchReligion pushed this belief that mind belonged to God etc Renaissance began to question church and pull research from nature Descartes Al I p proposed dualism mInd and b0dy are separate Church had mInd BIOIogy had body How is the nervous system organized The concept that specific brain regions are responsible for different aspects of behavior and mental processes 19th century s nervous system function localized YesPhrenoogy You can figure out a person39s personalitytraits by the bumps in their brain NoFlourens Doesn t matter where in the brain you lose function the loss of function is related to the overall brain ossgtBrought idea that brain was unified not localized YesBellMagendie Law Found that motorfiberssensory fibers in spinal cord would control different sides of the body depending on location YesBroca39s area Studied older people with strokes and found common region in brain associated with language production 0 Modern day Nervous system function is localized and distributed What is the basic unit of the NS quotNeural netquot Golgi idea that it was a net that all communicated with each other wrong 0 Ramon y Cajal Neuron is basic unit of nervous system right How does the nervous system give rise to behavior 0 1949 Hebb published 39The Organization of Behavior39 1991fMR allowed us to see brain in action Approachesin Bio psych Many divisions ie cognitive neuroscience neuropsychology Converging operations take best part of all divisions to get best idea of how brain works 0 Scientific inference Pure and Applied Research 0 Human and nonhuman research 0 Ethical considerations Sensorimotor System Monday August 17 2015 1239 PM Receptors gt Thalamic relay nuclei gtPrimary sensory cortex gtSecondary sensory cortex Association cortex start at receptors gt association cortex Visual System DorsalVentral Many V2V4 MT 1 LGN Photo receptors lt Motor System start at association cortexgtreceptors SMA Receptors M otor u n it Posterior Parietal Cortex PPC 0 PPC adapts to sensory changes 0 Intention to act 0 Apraxia inability to perform purposeful movements when asked Secondary Motor Cortex 0 Secondary motor area SMA Volitional movement encodes sequences of movemeI 0 Premotorcortex PMdPMv programs movements encodes spatial components of movements 0 Plays a role in not just performing action but also observing action neurons that fire in responseto performing a goaldirected movement and observing the same goaldirected movement I Originally found in ventral premotor cortex PMv of monkeys o The Myth of mirror neurons Scientists and others have extrapolated this origir finding to suggest a causal role for mirrors in action understanding human em and autism 39 Ex Seeing someone crying will make you feel empathy o Nota lot of evidence to support idea that mirror neurons can help autism Primary Motor Cortex Central sulcus middle separating motorright and sensory left 0 Different locations on the body are represented by different areas of motor cortex 0 Motor homunculusquotlittle humanquot 0 Contralateral control left motor cortex represents right side of the body and r motorcortex controls body parts on right side 0 May also represent other aspects of movement such as movement or target directic O Topographic Organization 0 Nearby parts of neocortex represent spatially nearby stimuli o Neural quotmapsquot that are highly efficient nts 1a pathy ight n 0 Visual svstem Retinotopy represents contralateral visual field fovea is overreprese bc it allows for high acuity vision more detail Auditorv svstem Tonotopy represents frequency lose higher frequencies as we age Somatosensorv svstem Somatosensory homunculus represents contralateral body more sensitive areas are overrepresented Sensorimotorsvstem Motor homunculus represents contralateral body parts bod used for intricate movements are overrepresented Cerebellum 0 quotLittle brainquot 0 Contains over half of the brain39s neurons Motorcoordination and balance Cerebellar ataxia Inability to coordinate movements Diverse sensory cognitive and emotional functions Basal Ganglia Complex loop connecting different areas of cortex 0 Role in action planning and sequencing movements Nonmotorfunctions as well 0 Helps motorcortex plan action Spinal Circuits Innervating muscles Neuromuscularjunction chemical synapse between motor neuron and muscle fiber 0 Involvesacetylcholine Motor unit singe motorneuron and all fibers it innervates 0 Can have a lot of motor neurons doing a lot of different things 0 Motor pool all neurons that innervate single muscle Spinal Circuits Patellar tendon kneejerk Reflex Spinal Cord and PNS Monosynaptic one afferent sensory and one efferent motor neuron Rap occurs here i nted parts yparts The rap on the knee tendon stretches the Spindles ol the thigh muscle and elicits a burst of tiring in their afferent neurons Spinal Circuits Voluntary movement Brain Spinal Cord and PNS T Rap occurs here The burst of firing in the spindle afferent neurons triggers a burst of firing in the thigh muscle motor neurons which causes the thigh muscle to contract 0 When you touch something hot and yourhand has already moved away by the you realize it was hot 0 The brain receives sensory input and computes relevant motorcommands Spinal cord carries out commands sent from brain 0 A continual process Sensorimotor Learning Chunkinggroupingindividualmovements Learning a motortask can quottransferquot control from higher to lower levels ofCNS Less brain activity during wellpracticed movements more efficient Paralysis of movement 0 Motor neuron disease ALS Amyotrophic Lateral Sclerosis Muscular dystrophy Spinal cord injury a time Learning amp Memory TuesdaySepu nber 82015 L12 HM 1241 PM Suffered from severe epilepsy of the medial temporal lobe MTL Hippocampus and surrounding MTL in both hemispheres were surgically removed Impairment for new declarative memories Amnesia Retrograde amnesia can39t remember memories from before brain jury Anterograde amnesia can39t form new memories after brain injury HM had anterograde amnesia and partial retrograde amnesia 3 years before surgery KC episodic amnesia after motorcycle accident Amnesia Ex no memory of infancy Sudden onset of severe anterograde and moderate retrograde amnesia last 46 hours damage to basal forebrain prefrontal cortex and hippocampus 0 major anterograde and retrograde amnesia 0 general memory deficits dueto heavy alcohol consumption lesions to medial diencephalon o anterograde amnesia and retrograde amnesia gets worse over time amnesia following blow to the head level of anterograde and retrograde amnesia related to severity of blow A blow to the head produces coma When the victim regains consciousness there is a period of confusion When period of confusion ends the victim has retrograde amnesia for events that occurred during the period just before the blow and anterograde amnesia for events that occurred during the period of WNl O confusion Normal cognitive function gt retrograde amnesia gt BLOW TO HEAD gt coma gt confusion and anterograde amnesia gt normal cognitive fxn Amnesia Consolidation and Reconsolidation Transfer from working memory to longterm memory Leads to structural changes in synapses Hippocampus plays a role in consolidation but other regions involved more than previously thought a recalled memory enters an unstable state before being updated and strengthened again Amnesiaforwhat O conscious longterm memories 0 longterm memories that do not require COHSClOUS awa reness Memory systems 0 Working memory 0 Fxn hold info online 0 Explicit Declarative o Prefrontal cortex 0 Procedural memory 0 Fxn how to o ImplicitNondeclarative o Basal ganglia and cerebellum Episodic memory 0 Fxn personal events 0 Explicit Declarative o Hippocampusamp Medial Temporal Lobe memories for particular events or experiences in one39s life memories concerning facts and general knowledge Neurons of MTL Spatial memory memory for the environment and objects in space Involves the hippocampus and entorhinal cortex HI II 39 r I I 39 I 0 Place cells In nlppocampusrlrewnen In a certaln place In the enVIronment Firing is flexible for different environments and contexts Grid cells in entorhinal cortex fire when in a multiple places in the environment Importantfor navigation Neurons of MTL Evidence for headdirection cells border cells and speed cells 0 Jennifer Aniston neurons represent concepts fire when recognizing a certain person place etc Brain Damage Wednesday August 26 2015 1231 PM L1O Brain tumors 0 Tumor Group of cells growing independently ofthe rest ofthe body 0 Uncontrolled cell division in glial cells or meninges 0 Benign tumor easily removable little risk of growing into surrounding tissue ex Meningioma 0 Malignant tumor difficult to remove or destroy continues to grow into surrounding tissue ex Glioma Stroke 0 Cerebrovascular accident in which brain39s blood supply is interrupted 0 Cerebral hemorrhage Blood vessel ruptures or bleeds 0 Cerebral ischemia blood vessel becomes blocked 0 Overactive glutamate after stroke may be cause of lasting brain damage lscbemic stroke Hemorrhagic stroke A clot blocks blood ow Bleeding occurs inside or to an area of the brain around brain tissue glosedhead iniuries 0 When the skull is not penetrated or broken 0 Contusion bleeding in brain without laceration 0 Hematoma a bruise or collection of clotted blood Concussion when blow to head disrupts consciousness o Mild traumatic brain injurymTB o No obvious structural damage but lasting effects Headtohead collisions watch video Chronic traumatic encephalopathy Concussion testing video Other causes of brain damage Infections of the brain ex Meningitis Neu rotoxins ex Mercury poisoning Genetic factors ex Down syndrome Programmed cell death ex Apoptosis Epilepsy uncontrolled electrical disturbances quotstormsquot in the brain disorder defined by repetitive unprovoked seizures Can have a seizure without epilepsy Can be detected by EEG do not involve entire brain 0 Simple in sensory or motor regions 0 Complex in temporal lobe temporal lobe epilepsy involve entire brain 0 Petit Mal disruption in cosnciousness vacant look 0 Grand Mal loss in consciousnessviolent convulsions Parkinson39s Disease Progressive movement disorder Onset around age 5060 Main symptoms 0 Tremor at rest 0 Bradykinesia o Muscular rigidity Reduced dopamine in substantia nigra and basal ganglia MPTP model mimics Parkinson39s symptoms Common treatment LDopa and other dopamine agonists Loss ofdopamine in substantia nigra leads to hyperactivity in the subthalamic nucleus of the basal ganglia leading to unwanted actions Lesion to subthalamic nucleus reverses Parkinson39s symptoms 0 Deep Brain Stimulation stimulates subthalamic nucleus to mimic lesion 0 Lasts 35 years Huntington39s Disease 0 Progressive inherited movement disorder Symptomszjerky movements lack of coordination Eventually leads to severe deterioration of mental and physical abilities Huntingtin gene autosomal dominant for Huntington39s disease Alzheimer39s Disease 0 Most common type of dementia Main symptoms 0 Initially forgetfulness anxiety loss of speech function 0 Eventually tota dementia inability to swallow Due to neuronal loss or atrophy along with buildup of amyoid plaques and neurofibrillary tangles Genetic component Amyloid hypothesis amyoid plaques are primary cause and they cause other symptoms Neural reorganization If motor neurons to rat whiskers are cut they reorganize to activate other muscles 0 Visual cortex is active in blind patients during braille reading and verbal memory tasks Treating CNS damage Neurotransplantation e adut neural stem cells 0 Visual training Constraintinduced therapy 0 Mirror box therapy for phantomlimb pain Neurotransmission Monday August 10 2015 1233 PM Types of action potentials EPSP depolarization PSPhyperpolarize Manipulating Action Potentials Lidocaine local anesthetic Optogenetics video Conduction ofthe Action Potential 0 Wave of excitation Does not degrade as it travels along the axon Relatively slow in unmyelinated axons fasterin bigger axons Myelin insulates the axon by preventing K leakage out 0 New action potentials are triggered at Node of Ranvier o Called quotSaltatory Conductionquot Upto 15 times faster than unmyelinated axons o Myelination is speeding up the rate of transmission 0 Multiple sclerosis MSAutoimmunediseasein which myelin is degraded weakened conduction Learning new motor skills requires myelin strengthened conduction Diversity of CNS Neural Conduction The HodgkinHuxley Model ofneural conduction is based on a motor neurons in the PNS of a squid The original model does not account for many new findings in CNS neurons 0 Ex The rate of firing varies greatly across different types of CNS neurons The nervous system is connected through synaptictransmission Synapse complex precisely organized nanoscale structure through which two neurons communicate 0 Electrical synapsegapjunction 0 Chemical synapses 39 Axoaxonic synapse 39 There are many different types of chemical synapses Neu rotransmitterAction Synthesis and Storage A chemical gas or hormonethat is synthesized in and released from a neuron Synthesized in cell bodylarge NTs or cytoplasm small NTs Stored in vesicles Coexistence small and large NTs at same axon terminal NeurotransmitterAction Release the process ofa vesicle fusing with presynaptic membrane and releasing a neurotransmitter into the synaptic cleft Small NTs released every action potential 0 Large NTs released after multiple action potentials Neu rotransmitterAction Receptors onotropicopen ligandgated ion channels Metabotropic opens Gproteingated ion channels 0 regulates exocytosis Neu rotransmitterAction Deactivation Reuptake NT taken back inside presynaptic neuron Enzymatic degradation NT broken down after release Diffusion NT moves out of synaptic cleft NeurotransmitterAction Summary Seven Steps In Neurotransmltter Action Neurotransmitter gc 39 gf g Synthcslzmg molecules we synthesized 1 a mums ltom precursors undertho g In uence ol enzymes N 39 Neurotmmmmm Neurotransmitter 39 o Vocwws molecules are stored in vesncles Vesvde Neurotransmitter molecmes that weak lrom their VOSlCIOS are destroyed by enzymes Degmdmg enzymes Acton potentials cause vesmles to less Wllh the presynaptic membrane and release their neurotransmitter molecules into the synapse Released neurotransmitter molecules bind with autoreoeptom and inhibit subsequent neurotransmitter release Released neurotransmitter molecules bind to postsynaptic receptors Released neurotransmitter molecules are deactivated by either reuptake or enzymatic degradation 1SynthesB 23 Storage 4 Exocytosis 56 Receptor binding 7 Deactivation Neu ropharmacology Drug effects 0 Agonistzfacilitate a NT39s effects mimic 0 Antagonist reduce a NT39s effects block Drugs act on partial list Synthesb Release Receptors Reu ptake Taking drugs effects the successful completion of processes Some Mechanisms ot Drug Action Agonistic Drug Effects Antagonistic Drug Effects Drug increases the synthesis of Drug blocks the synthesis oi neurotransmitter molecules neurotransrnltter molecules eg by increasing the amount eg by destroying oi precursor synthesizing enzymes Drug increases the number oi neurotransmitter molecules by destroying degrading enzymes Drug causes the neurotransmitter molecules to leak trom the vesicles and be destroyed by degrading enzymes Drug increases the release of neurotransmitter molecules from terminal buttons Drug blocks the release of the neurotransmitter molecules from terminal buttons Drug binds to autoreceptors and blocks theirinhlbitory etiect on neurotransmitter release Drug I ms autor m8 and inhibits neurotransmitter Drug binds to postsynaptic release receptors and either activates them or increases the effect on them oi neurotransmitter Drug is a receptor blocker molecules it binds to the postsynaptic receptors and blocks the effect 03909 bloc the WWWquot 0 of the neurotransmitter neurotransmitter molecules by biocking degradation or reuptake Types Of n eu rotra ns m itters SmallMolecule Neurotransmitters Dopamine Catechoiamines Epinephrine Monoamines Norepinephrine Indolamines Serotonin Acetylcholine Acetylcholine LargeMolecule Neurotransmitter Amino acids 0 Glutamate major excitatory neurotransmitter 0 GABA major inhibitory neurotransmitter Acetylcholine 0 Small molecule NT 0 Mostly in ANS at neuromuscularjunction 0 Deactivated by enzymatic degradation 0 Two main receptors nicotinic and muscarinic 0 Cholinergic pathways learning and memory Monoamines 0 Madefrom a single amino acid MONOamines Dopamine Epinephrine and Norepinephrine synthesized from the amino acid tyrosine Serotonin synthesized from the amino acid tryptophan o Cocaine is a serotonin norepinephrine and dopamine reuptake inhibitor Tyrosine 39 A7 Ldopa Dopamlne I Norepinephrine Epinephrine Dopamine Dopaminergic pathways motorcontrol reward and learning 0 Ldopa synthesizes into dopamine see image above Norepinephrine Noradrenergic pathways mood arousal and sexual behavior Serotonin Serotonergic pathways sleep mood and anxiety 0 Ecstasy attaches to serotonin transporters so serotonin can39t be transported back so this leads to elevated moods and heightened perceptions eventually affects internal regulation faster heart rate muscle spasms internal temperature THEMES STRUCTUREFUNCTION o The bigger the axon the faster neural conduction myelin axon with also increase rate 0 Type of neurotransmitter affects different processes PLASTICITY 0 Using drugs like ecstasy affects how neurotransmitters are release and synthesized can be both long term and short term 1 o It an axon is myelinated or not attects tor example the learning ability in a person with multisclerosis NEW RESEARCH Evolution amp Genetics Review Monday August 24 2015 1229 PM Evolution amp Genetics Review 0 Behavior interaction between genes experience and current situation 0 Darwin and natural selection Courtship displaysmate bonding as evidence for evolution of behavior 0 Human brain has increased in size mostlyin cortex and convolutions over course of evolution 0 No clear relationship between brain size and intelligence but larger brains may support capacity for a wider variety of cognitive skills and specialized organization Mendelian genetics genes and traits DNA replication can lead to gene mutations gene expression depends on both genes and environment Epigenetics study ofall mechanisms that influence gene expression without changing the genes themselves methyl group CH3 attached to DNA Studying influence of genes Genetic engineering Knockout remove DNAforthe gene or knockin add in different DNAfor a gene mice 0 Can directly study effects of gene on phenotype Twin studies Monozygotic identical twins 100 genetic overlap Dizygotic fraternal twins or nontwin siblings have 50 genetic overlap estimate of how much variability in a particular trait can be attributed to genetic variation in that study 0 0al due to experience 0 1due to genetic variation 0 Minnesota study of twins reared apart and Turkheimer et al 2003 Themes Neu roplasticityThe nervous system adapts and changes itself over time Drugs amp Reward VVednesdayAugust262015 L11 1231PM Basic principle of drug effects Consumed via ingestion injection inhalation or absorption Must pass bloodbrain barrier to enter CNS Acts diffusely ie anesthetics or on specific NT receptors ie SSRIs Drug effects often terminated by their metabolism Agonists facilitate an NT39s effects mimic and antagonists reduce an NT39s effects block Can affect any stage of NT action synthesis storage release receptors and deactivation Many individual differences in a drugs39 effects decreased sensitivity to drug effects after prior exposure sensitization increased sensitivity tolerance higher in environments associated with taking the drug 0 New environments increase risk of overdose I elimination of drug can lead to behavioral effects opposite to the initial drug effects 0 Withdrawal symptoms suggest physical dependence on drug addicts take drugs to avoid withdrawal symptoms Reward paradigms Intracranial selfstimulation repeatedly administering brief bursts of electrical stimulation to specific region in an animal39s own brain Selfstimulate to activate reward circuits Reward systems reward circuit where dopamineis main neurotransmitter Dopamine is mainly in ventral tegmental area which projects to the nucleus accumbens Reward systems and addiction 0 Drug addict a habitual drug user 0 Positive incentive value quotwantquot Hedonic value quotlikequot anticipated pleasure want motivates behavior Dopamine release in NAcc follows signal that predicts reward Similar effects forthe other types of addictions ie overeating gambling Relapse often due to stress drug priming or conditioned environmental cues cues longer after withdrawal elicit more craving Improving environment decreases risk of relapse Commonly abused drugs Hallucinogenic drugs 0 Ex ecstasy MDMA LSD mescaline peyote cactus PSP 0 Users develop low tolerance low addiction potential 0 Most are serotonin agonists o Ecstasy increases serotonin release and destroys axons Stimulants 0 Ex cocaine meth ecstacy adderall caffeine 0 Very addictive mild withdrawal 0 Cocaine inhibits dopamine reuptake 0 Structural changes with meth use Opiates 0 Ex morphine codeine and heroin 0 Very addictive users develop high tolerance 0 Act on receptors that normally bind endogenous opiates endorphins Tobacco o 10 ofdeaths worldwide 0 Users develop nicotine addiction quickly 0 Complicated effect on neurotransmission o Addiction has genetic component 0 Alcohol 0 Depressant and stimulant 0 Many develop tolerance wide range ofwithdrawal symptoms 0 Ethanol affects Ca2 2nOI messengers and GABAglutamate transmission 0 Korsakoff39s syndrome and fetal alcohol syndrome Korsakoff39s brain disorder of loss of shortterm memory exploited by alcohol bc of thiamine deficiency Marijuana O Acts on cannabinoid receptors in basal ganglia cerebelllum and hippocampus Low addiction potential low likelihood ofwithdrawal symptoms Associated with increase in gray matter in NAcc Neurophysiology Wednesday August 5 2015 1236 PM Week 1 Wednesday White matter microstructure throughout the brain correlates with visual imagery in grapheme Neural communication an electrochemical process 1 A presynaptic and postsynaptic neuron at rest 2 The presynaptic neuron communicated to the postsyaptic neuron by releasing neu rotran 3 Receptors in the dendrite of the postsynaptic neuron receive the neurotransmitters dep 4 finish slides on GS Neuron cell membrane allows some substances to pass but not others two layers of linked fatty molecules pore in membrane that lets certain molecules pass when open transfers a signal to the inside of a neuron when certain molecules ie ne Membrane potential An atom or molecule that has acquired an electrical charge by gaining or losing onelt the difference in electrical charge between the inside and outsidec Factors contributing to RM P 1 Concentration gradient particles in random motion tend to move from areas ofhigh con a Like when you spray cologne and the smell goes all over the room 2 Electrostatic pressure like charges repel each other and opposite charges attract each 01 3 Permeability ofthe membrane the ion channels contributing to the membrane potentia passive process does not require energy 4 Active ion transport NaK pump a transporterthat uses energy to pump 3 Na out 0 energy this is an active process Ion Movement at Rest Concentrations at rest Potassium K Sodium Na Chloride Cl Inside Outside 400 20 50 440 40 150 560 ecolor synesthesia Ismitters across the synapse olarizing the membrane cell wall eu rotransmitters bind to them Dr more electrons of the neuron centration to areas Of lOW concentration her l are voltagegated This kind ofopening and closing is a fthe neuron for every 2 K into the neuron Since it requires 02 Wa nts in Wa nts C ut Wa nts in u Wa nts in Wa nts in Wa nts out in liiiiwi H iii Closed So me o pen 0 pen H gt Eff P u m p ed 0 u t P u m p ed in N o n e Polarizing the neuron membrane changes in the membrane potential produced by the action ofni Excitatory postsynaptic potential EPSP depolarization increase likelihood a neuron wi Inhibitory postsynaptic potential IPSP hyperpolarization increase likelihood a neuron PSPs are graded they are transmitted decrementally and they are transmitted rapidly Images on gauchospace the integration of PSPs arriving at different parts ofthe neuron o NeuronsA and B activate excitatory receptors EPSP o NeuronsC and D activate inhibitory receptors IPSP 39 What happens when neuronsA and C fire simultaneously III They cancel each other out 0 the integration of PSPs arriving at different times 0 Neuron A activates excitatory receptors EPSP o Neuron B activates inhibitory receptors IPSP Massive momentary 1 ms reversal of the membrane potential 50 mV quotAllornonequot Generated at axon hillock and propagates down entire axon 60 50 An EPSP and an 40 Action Potential 30 20 10 0 1 O 20 3O 4O 50 EPSP 450 L 70 80 90 n Action potential Membrane Potential millivolts Timn lmillicnnnndc eurotransmitters released by presynaptic neurons ill fire will fire I 39IIW I I I I I l39mV39ng STIMULUS 60 Sodium 50 channels M 76 close 395 30 REPOLARIZATION 31 10 Potassium O 3 Channels HYPERPOLARIZATION a a 10 open C E E s d39 392 V 30 C arlggls Potassium q n channels 2 50 ope start to close l 1 2 3 4 5 Time milliseconds rising phase and repolarization It39s impossible to fire another action potential hyperpolarization Need a greater signal than normal for an action potential to happen again Summary 0 Voltagegated Na channels open 0 Na ions rush into neuron 0 The membrane potential becomes more positive 0 Voltagegated K channels open 0 Voltagegated sodium channels close 0 Potassium ions leak out ofthe neuron 0 The membrane potential becomes negative again 0 End ofthe refractory period TnIvnnl nnn ICLI UUULUAIII I IA Pufferfish fugu is considered a delicacy in Japan Pufferfish produce TTX a selective Na channel blocker Blocked Na channels no Na influx no action potentials DEATH Perception and Attention Wednesday August 12 2015 1254 PM Sensory Systems 0 Association cortex 0 Secondary sensory cortex 0 Primary sensory cortex Thalamic relay nuclei Receptors Flow ofVisual Information Retinageniculatestriate pathway 0 Crosses at optic chiasm Retinocollicular pathway Motion perception Middle temporal area MT Motion aftereffect Due to lessened responses of motionselective neurons over time Akinetopsia quotmotion blindnessquot Visual Recognition Visual agnosia deficit in visual object recognition 0 Ex A man mistaking his wife fora hat 0 You can see the objects completely fine youjust cant recognize the object 39 Prosopagnosia visual agnosia for faces onlygt Fusiform Face Area FFA gets damaged which leads to the prosopagnosia Selective Attention Hemispatial neglect deficit in attention to contralateral side of space 0 Due to damage in posterior parietal cortexusuallyfrom a stroke often temporary 0 Ex Drawing only half a clock half a house etc because they don t believe other half exists 0 They completely forget about the left side oftheir visual field 0 Change blindnessif attention is on different spot you wont see something very obvious 0 Ex video with kids where you count passing ball and gorilla walks in unnoticed Auditory system Hair cells organ of corti gt Inferiorcolliculus gt Medial geniculus thalamus gt Auditory cortex A1 temporal lobe Association cortex 0 Secondary sensory cortex 0 Primary senesory cortex Thalamic Relay nuclei Receptors The ear Physical dimension Perceptual dimension Amplitude Loudness Frequency Pitch Complexity Timbre Vibrations are turned into electrical signal Different hair cells bend depending on their amount and location Tonotopy Both the organ of Corti and auditory cortex have tonotopic organization 0 Location of excitation related to the frequency ofthe sound 0 We lose ability to hear higher frequencies first as early as children and then lower frequencies as we age Deafness Due to damage to ossicles or the cochleaauditory nerve Auditory cortex damage does not cause deafness Cochlear implants convert sound directly to electrical signals 0 Can get an implant as young as 12 months it bypasses the cochlea and transmits what you hear into pattern of electrical impulses to auditory cranial nerve Somatosensory system Cutaneous receptorsgt Ventral posterior lthalamusgt SI 0 Association cortex Posterior pa riteal some frontal areas 0 Secondary sensory cortex 0 Primary sensory cortex Thalamus relay nuclei Receptors Touch pain knowing where you are in spacewhere your body is blood pressure all somatosensory system Skin receptors Vary in receptive field size large vs small Vary in rate of adaptation fast vs slow 0 Will immediately start firing if touch something different you continue touching the same thing they will slow 7 o pain and temperature Dermatomes Dermatomes parts ofthe body served by one segment of the spinal cord Rashes in specific area related to damage to corresponding spinal cord segment Somatosensory Pathways Touch and proprioception pathway crosses at medulla Pain and temperature pathway crosses immediately Somatosensory homunculus Touch perception to different body parts is organized on primary somatosensory cortex 0 Not dependent on size of body part dependent on sensitivity of body part 0 Phantom limb sensation that absent limb is still attached Topographic organization 0 Nearby parts of neocortex represent spatially nearby stimuli o Neual quotmapsquot 0 Visual system Retinotopy Development Monday August 24 2015 1229 PM Phases of neurodevelopment Cell Fertilization and division 0 one cell divides into two gametes each with one chromosome of each pair 0 one cell divides into two each with pair of chromosomes Daughter nuclei ll Daughter nuclei Interphase Meiosis I Homologous Meiosis II chromosomes 0 Zygote original cell 0 Begins to divide o Totipotent can become any cells o Pluripotent can become most cells Induction of neural plate 0 At this point cells are mostly multipotent can become any related cell 0 Unipotent cells can become only one cell type Neural tube defects 39 Frontal end of tube does not close brain fails to develop almost always fatal Back end oftu be does not close spine does not form properly can be surgically corrected Cell proliferation amp migration 0 Npllml nrnlifpmtinw rpll nllmhprinrrpncpc arpntlv I vvllul rllvlllvlublvlllvvll IIVIIIIMVI IIIVIVMUVU Dlvubl Cell division mostly in ventricular zone 0 Migration to appropriate target location depends on time and location that new cell arises Cell goes to targets via tangential and radial migration Cell migration 0 extension grows and follows attractive cues Gliamediated migration cells move along temporary radial glial network Axon growth amp synapse formation certain genes begin to express so neurons start to acquire distinctive appearance and connections directs axon growth formation of new synapses facilitated by astrocytes o Astrocytes very important to ensure survival make sure once synapses develop they will stay that way Synaptic Pruning extra neurons and synapses eliminated to increase efficiency programmed cell death 0 After cell death a more focused pattern of synaptic connections develops Postnatal growth Synaptogenesissecretion of new synapses Myelinationincreases speed of conduction of synapses Dendritic branchingfacilitating more possibilities for more synapses Development ofthe Prefrontal cortex 0 Last region to develop 0 Working memory planning actions and response inhibition among other functions uncontrollable repetition of a response due to lack of inhibitory control Effect of experience experience must occur within a particular interval experience can still have effect outside interval Sensory deprivation quotuse it or lose itquot Monoculardeprivation Horizontal ampvertical cats Psychiatric Disorders Tuesday September 8 2015 1241 PM 45 multiple choice and tf C15 90 pts 2nd half of course 1 short answer 10 pts definition example for how it plays out in brain relate to neuroplasticity how it relates to the brain changing learning etc Almost all the C15 relate to conceptsinfo from lecture Bring pink par score form pencil photo ID Psychiatric disorders Psychological disorder severe enough to require treatment Psychiatrist psychologist who can prescribe drugs for patients Diagnoses governed by DSM5book where if you match certain of symptoms you can be diagnosed as 0 About 1 in 5 US adults 437 million experience mental illness in a given year Pharmacotherapv 0 The use of pharmaceutical agents to treat illness 0 studies conducted on humans to assess therapeutic efficacy of a drug or other treatment 0 Placebos control substance 0 Active placebos placebo with similar side effects as test drug TABLE 182 Phases of Drug Development BASIC RESEARCH I 0 Discovery of the drug development of efficient methods quot39f WhOIe process takes of synthesis and testing with animal models millions Of dollars and a to n of time Application to begin clinical trials and the review of basic research by government agency HUMAN CLINICAL TRIALS Phase 1 Screening for safety and finding the maximum safe dose 39 Phase 2 Establishing most effective doses and schedules of treatment Phase 3 Clear demonstrations that the drug is therapeutic Application to begin marketing and reviews of results of clinical trials by government agency SELLING TO THE PUBLIC Recovering development costs and continuing to monitor the safety of the drug Source Based on Ztvm 2000 The chemical imbalance mvth of mental illness Pharmacotherapy essentially treats psychiatric illness as a physical problem 0 Ifneurotransmission is lowgt elevate it o Ifneurotransmission is high gt reduce it Neu rotransmission plays a role but there is no evidence psychiatric disorders are caused by a chemical imbalance 0 Only small role Affective disorders Disturbances of mood or emotion severely depressed mood that persists for at least two weeks difficult to perform daily essential tasks 0 Can be triggered by a negative experience doesn t need to be triggered by external stimulus can have random onset a high energy overactive and impulsive state 0 Symptoms can be racing thoughts fast speech high energy 0 Not usually singular disorder usually in association with bipolar intermixed periods ofdepression and mania 7 0 Strong genetic and environmental components 0 Concordance rate if both twins have a trait that s the rate Identical twins have 60 chance of getting depression if other has it 15 forfraternal twins 0 Stress or negative events may trigger depression 0 Seasonal effective disorder when it becomes colder winter more likely to be depressed o Postpartum depression after giving birth mother might develop depression by feeling detached from the baby and not being able to cope with new life Treatment for affective disorders 0 first class ofantidepressant drugs monoamine agonIst can lead to dangerous Increase In blood pressure 0 MAO breaks down and reduces of neurotransmitters o Inhibitors stop MAO block serotonin and norepinephrine reuptake 0 Blocks reu ptake of neurotransmitters to make them stay in synapse first mood stabilizer treats mania without increasing depression selectively blocks serotonin reu ptake elective erotonin eu ptake inhibitors selectively blocks norepinephrine reu ptake Monoaminetheory ofdepression that depression is associated with the underactivity at serotonergic and noradrenergic synapses o A lot of people sufferingfrom depression aren39t helped by the SSRI and SN Rls SSRls do not show alleviating effects until weeks after treatment Neu roplasticity theory of depression depression is associated with reduced neu roplasticity SSRls may promote neu rogenesis which takes weeks Drawbacks of antidepressants 0 Usually only helps people who are extremely super depressed Nonpharmacologicaltreatments 0 Cognitive behavioral therapy shortterm therapy focusing on changing patterns of thinking or behavior 0 Brain stimulation stimulation to anterior cingulate gyrus can alleviate depressive symptoms Anxietv disorders 0 Fear that disrupts normal functioning in the absence ofa direct threat 0 Main symptoms 0 Fear and worry 0 Tachycardia rapid heartbeat 0 Nausea 0 Sleep disturbances Obvious environmental component but genetic as well stress response in the absence of an obvious stimulus caused by exposure to a specific object A r AAAIAA nnAllA IAAM A U EX leUbUUpHUUId bEEIHg d blldKE ICC UI llElgHLb rapidonset attacks of extreme fear frequently recurring uncontrollable anxiety producing thoughts and compensatory responses 0 Germobsessionhandwashingcompulsion persistent distress following exposure to extreme stress Treatment for anxiety disorders Benzodiazepines eg Valium increases binding of GABAA to its receptor Serotonergic systems may also be involved 0 Anxiety often cooccu rs with depression Mrette svnglrome Disorder characterized by tics involuntary repetitive movements and vocalizations Main symptoms 0 Motortics lewd gestures hitting touching 0 Vocal tics barking grunting obscenities About3 times more likely in males than females 0 Treatment neuroleptic drugs dopamine antagonist block dopamine o Suggests abnormalities in dopaminergic pathways involving basal ganglia Schizophrenia Psychiatric disorder that has to due with abnormal social behavior distorted reality what is real what is no Literally means quotsplitting a brainquot 0 Does not mean two identities or split brain 0 Positive symptoms excess of normal function 0 Delusions hallucinations incoherent thought odd behavior 39 Ex Scratching bug not on arm thinking CIA is following you 39 Usually always auditory hallucinations visual very very rare 0 Negative symptoms loss of normal function 0 Affectiveflatteningabsence of emotional expression 0 Anhedoniain ability to feel pressure 0 Catatoniastateofimmobility Overall prevalence 1 of population 0 Strong genetic basis Concordance rate in monozygotic twins is 45 dizygotic twins is 10 0 Genetic predisposition may or may not be activated by experience 0 Environmental trigger smoking a lot of weed hallucogenics ESPECIALLY if have relative Ali39l39h crhi7nnhrani2 VVILII JUIIILUPIIICIIICI Brain alterations o Smaller cortex and enlarged ventricles 0 Less gray matter Treatment for schizophrenia First ant schizophrenic drugs chlorpromazine and reserpine Therapeutic effects within 23 weeks Side effects mild tremors and muscular rigidity like Parkinson39s disease Theories of schizoph renia D1 and D2 receptors dopamine receptors Dopamine theory of schizophrenia schizophrenia is related to excessive dopamine activation of D2 receptors Chlorpromazine and reserpine are D2 D receptor blockers Glutamate GABA and serotonin have been implicated in schizophrenia New mouse model of schizophrenia o Knockout mice for gene Arp23 o Resulted in schizophrenic behavior 0 Found excessive dopamine hyperactive frontal neurons and fewer dendritic spines Language Tuesday September 8 2015 1243 PM L14 Lateralization of function Lateralization emerged in vertebrates 500 million years ago 0 More efficient for neurons performing a particular function to be concentrated in one hemisphere Lateralization of a fxn does not mean that fxn is exclusively in one hemisphere or the other Split brain Myersamp Sperry Info travels between hemispheres via corpus callosum Without corpus callosu m the two hemispheres operate independently and learning cannot transfer Sperry amp Gazzaniga Brief flash 100 msto one visualfield Right hand respondsforthe left hemisphere and vice versa Verbal responses for left hemisphere only Cerebral specialization Left hemisphere o Ipsilateral movement 0 Language 0 Interpretation of events 0 Right hemisphere 0 Spatial ability 0 Emotions 0 Music 0 Current perspectives o In splitbrain patients some info like emotional content can still be transferred bw hemispheres o More difficult tasks recruit both hemispheres more 0 Mental abilities lie language Spatial abilitv music have manv different U U I cognitive components Each component may have its own lateralization Language acquisition 0 We are born with the capacity to learn language Primates cannot be taughtto use language as humans use it 0 Critical period forlanguage development 0 At 10 months human infants say little and can distinguish the sounds of aHlanguages 0 At 30 months they can speak a lot and can distinguish only their own language 0 Cortical localization oflanguage an impairment in expressive language 0 an impairment in receptive language WernickeGeschwind model Broca39s area language production Wernicke39s area language comprehension Angular gyrus languagerelated visual input Arcuate fasciculus white matter pathway connecting Wernicke39s to Broca39s How the model works Responding to a question heard A1 analyzes sound Wernicke39s determines what was said Arcuate fasciculus Broca39s forms motor plan M1 implements plan Reading aloud V1 analyzes image Angular gyrus relates visual form to spoken form Wernicke39s determines what was said Arcuate fasciculus Broca39s forms motor plan 11 M1 implements plan 0 Damage to angular gyrus o inability to read 0 inability to write OPP N OWPP NPO Damage to arcuate fasiculus o poor speech repetition 0 Absent connections in people who stutter Arguments against model 0 Damage to Broca39s or Wernicke39s sometimes has little effect on language 0 Brain damage beyond Broca39s and Wernicke39s can disrupt language individual variability o Broca39s and Wernicke39s aphasia rarely exists in pure forms 0 Broca39s area goes silent during actual speech production Memory amp Emotion Tuesday September 8 2015 1241 PM How do we learn Learning depends on the plasticity of synaptic transmission Hebbian learning if neuron Atakes part in the firing of neuron B repeatedly and persistently then the strength between the two neurons is increased Donald Hebb 0 quotCells that fire together wire togetherquot Leads to an enduring increase in synaptic efficiency that may underlie longterm memory LongTerm Potentiation LTP LTP longlasting increase in synaptic strength seen with highintensity high frequency stimulation of the presynaptic neuron Longterm depression LTD reduction of synaptic strength seen with prolonged lowfrequency stimulation of the presynaptic neuron LTP commonly studied in the rat hippocampus Glutamate major excitatory neurotransmitter AMPA receptor ion channel lets Na ions in NMDA receptor ion channel lets Na and Ca2 ions in blocked by Mg2 when neuron is at rest Activation ofAM PA receptors depolarized cell gt drives Mg2 out of NMDA receptors allowing influx of Ca2 ions This influx activated protein kinases and enhances subsequent neurotransmitter release This change makes the postsynaptic neuron more responsive ie LTPincreased synaptic efficiency Role of LTP in memory There is LTP during both encodinginitial learning and consolidation of a memory Common view LTP is necessary for memory storage New view LTP is necessary for retrieving a memory o This view suggests a memory may never really be erased but become lost within a network of cells Phineas Gage In 1848 a tamping iron rammed into his face and through the top of his head Damaged his left frontal lobe Became aggressive and impulsivewas quotno longer Gagequot KluverBucy Syndrome Bilateral removal of temporal lobes in monkeys and cats Tame flattening of emotions fearless Failure to recognize common objects 0 Extreme oral tendencies Hypersexuality Mostly due to amygdala damage Papez Circuit Limbic system Proposalthat limbic system controls the expression of emotions by connections with hypothalamus Influenced by perception of emotions by connections with cortex Outdated view Theories of emotions o Perception of bear gt feeling of fear gt physiological reactions 0 Perception of bear gt physiological reactions gt feeling of fear 0 Perception of bear gt feeling of fear amp physiological reactions 0 Modern biopsychological view 0 All interconnected Emotionsamp Facial expressions Duchenne smile a genuine smile that involves muscles that can39t be controlled voluntarily Facial feedback hypothesis makinga happy face makes you happier Auditory fear conditioning Hears sound alone no physiological response 0 Sound paired with electric shock blood pressure increases stops moving Hears sound alone now blood pressure increases stops moving f amygdala is damaged after condition there is no longer a physiological response Lesions to MGN medial geniculate nucleus block fear conditioning Pathways from amygdala mediate defensive behaviors and fightorflight responses Contextual fear conditioning Develop fear for stimuli associated with fearinducing stimuli Involves amygdala and hippocampus Prefrontal cortex regulates fear response Neural mechanisms for human emotion Emotional experience governed by widespread interaction between many regions Prefrontal cortex is activated when consciously changing one39s emotional reaction Betablockers epinephrine receptors antagonists can disrupt emotional memories Emotions and memory 0 Normal adults remember pleasant and unpleasant pictures more than they remember neutral pictures 0 Patients with damage to the amygdala do not show this effect 0 The delusion that others or the self have been replaced by imposters Disconnection between ventral stream and amygdala Separate pathway between auditory cortex and visual cortex and amygdala why he believes them on phone but not in person VISIon Tuesday August 11 2015 1231 PM When we blink we have temporal integration because we39re not losing the picture of this visual world 0 Light electromagnetic radiation capable of stimulating human vision Human eye Eye muscle Ligament Iris Fovea Pupil Blind spot Lens Cornea Optic Ciliary newe muscle Sclera the white of the eye Retina the difference in image location ofan object seen by the left and right eyes Retina has 5 layers Each has Photo receptors are furthest awayfrom light but are first to receive light Amacrine Honzontal Cone Rod receptors receptors sendsinfo to brain Ibipoiarceils preprocesses info detects light 2 kinds of photoreceptors rods and cones Photoreceptor is a neuron that receives light Rods mainly in peripheral retina more active at night processes diffshades ofgrey Cones process diff colors RODS Scotopic system CON ES Photopic system 100 million 394 million Active in dim light Active in bright light One type rhodopsin Three types smallmediumlong Monochromatic info Color info Poor acuity Excellent acuity n I I I l A I I ll Peripheral retIna Central retIna tovea Visual Transduction Photoreceptor neuron that receives light not neurotransmitters as input Visual transduction conversion of light into neural signals What happens to rods in light vs dark h the DARK In tho LIGHT clt kc ULW 1 Lghl moms Rhaoaos n W563 x W are ec re I W Star rum 2 A a mull rn quot1 10quot m crumb close 0 Sodium non Sodaquot orquot 39 M cm ON 3920 Mo 39nth part4 y rods and O I 0001 u 39 N from town in rock become Wad 4 Guam release ismouced Rocs cert Jody recase 9123m32e In the dark the membrane potential is more depolarized that it would be in light In light rhodopsin is bleached which activates g protein and allows Na channels to close and leads to hyperpolarization Bigger the light the more hyperpolarization Color vision Trich romatic theory ability to perceive every color is mediated by 3 different cone receptors Opponent processing theory color vision depends on systems that produce opposite responses to light of different wavelengths Cone receptors maximally sensitive to different wavelengths Bipolar cells gt Excitation Inhibition Ganglion cells A Short Medium Long 420 nm 530nm 560 nm L r s nun M l l xi illv N 39 j l lquot I Y Blue vs yellow 1 Y Red vs 3 Brightnessdarkness green detectors Flow ofvisual information Q Retinageniculatestriate pathway Crosses at optic chiasm Retinocollicular pathway RetinagtThalamus LGNgtV Striate Your right sees your left your left sees your right Certain Fovea overrepresented Broad distribution of neurons active Lateral Geniculate Nucleus LGN 0 Parvocellular P cells layers 36 small process color and fine details 0 Magnocellular M cells layers 12 large process motion 0 Koniocellular K cells inbetween layers very small function unclear Lateral inhibitionContrast effects We can see edges between colors better than the actual colors themselves lateral inhibition interconnected neurons inhibit their neighbors and allows Receptive Fields 0 Receptive field of a neuron Area ofthe visual field that when stimulated can cause the neuron to fire 0 Receptive field properties become increasingly complex from retina to LGN to Visual Cortex OFF ll llllHlllllHllllllllllll H l The most effective way of maximizing the firing of an oncenter or offcenter cell is to completely illuminate either the on area or the off area of its receptive field If both areas of a cell s receptive field are illuminated together there is little reaction from the cell Know what happens when you39re shining light in terms ofonoff button On excitatory parts amp off inhibitory parts of cell Simple amp Complex cells Simple cells Complex cells Some ofVl cells MostofVl cells Monocular Binocular Responds to position Responds to orientation amp orientation regardless of position monocularonly responds to 1 eye Organization ofvisual cortex 0 Organized in vertical columns 0 Related columns are clustered an A Orientation columns Ocular dominance columns Novnoon twining the bum 3 t a Door Cannon v3 39avom C oppr0 0 mo LIOOMCOC lull0N l artmc Damage to V1 Visual cortex 0 Scotoma damage to V1 causes blindness in corresponding visual field nlll A A LI 43 AALAM AI IAA AAAAAAIAAIAIA AAAAA 39 DIIHUSIBHLZ Cd see SLIHIUII UBSPILE SCULUHICI dHU HU CONSCIOUS defEHESS


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