Biopsychology EXAM 1 STUDY GUIDE
Biopsychology EXAM 1 STUDY GUIDE
Popular in Course
Popular in Psychlogy
This 13 page Bundle was uploaded by Sierra Wollen on Sunday April 20, 2014. The Bundle belongs to a course at University of Washington taught by a professor in Fall. Since its upload, it has received 449 views.
Reviews for Biopsychology EXAM 1 STUDY GUIDE
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 04/20/14
Biopsychology FINAL Study Guide for Exam 1 L content was only in lecture T content is only in your textbook LECTURES 331 42 AND CHAPTER 1 Neuroscience T The scientific study of the neurosystem Divided into many categories including biological psychology Biological psychology T The study of the biological bases of psychological processes and behavior Persistent issues in biopsych L Mind v Brain localization of function neural communication Mind versus brain Descartes Dualism A debate first brought about by early philosophers namely Rene Descartes The early question was whether the mind and the body were separate entities Now biological psychologists want to know how the brain produces the mind A philosopher in the 1600s who is famous for his idea of dualism as well as his primitive speculations about nerves and re exes The idea that humans are comprised of a material bodybrain and an immaterial mind or soul Dualism is widely rejected by biological psychologists who believe the brain produces the mind but are not yet sure how Localization of function The idea that different brain regions specialize in specific behaviors Localization is complicated because neurons communicate across regions Support for localization 0 Lesion studies when one part of brain is damaged a behavior is affected 0 It is possible to measure peaks of function in certain brain areas 0 The success of TMS Transcranial magnetic stimulation proves it is possible to impede certain behaviors when specific brain areas are stimulated o Localization is complicated because neurons communicate across regions Lesion studies L A technique in which an area of the brain is damaged in order to see the resultant change in behavior supports localization of function Phrenology A pseudoscientific fad in which people believed that bumps on the skull were due to enlargement of brain areas responsible for certain behaviors Neuroplasticity Ability of the nervous system to change in response to experience or environment Neural communication Neurons are discrete entities that communicate electrically within the cell and chemical between cells Need to find out how electrical and chemical processes allow communication within and btwn neurons and thus create our conscious experience Santiago Ramon y Caj al L quotNeural Doctrinequot L Used Golgi Stain stains small of whole neurons and discovered the Neural Doctrine Set of facts discovered by Cajal about neurons 0 Neurons are structuralfunctional units of nervous system 0 Neurons are discrete entities 0 Cell bodies axons dendrites 0 Action potentials are directional Somatic intervention T Manipulates body structurefunction and observes resultant changes in behavior 0 Ex lesion studies Independent variable T Dependent variable T Factor that is manipulated 0 Ex in lesion study brain damage created Factor measured to monitor change in response to independent variable 0 Ex behavior change due to lesion Behavioral intervention T Alter or control behavior and observe resultant changes in body structure 0 Indp V behavior 0 Dept V body change Correlation T Quantifies cooccurrence of behavior and somatic change Negative correlation measure 1 goes up while measure 2 goes down vise versa Positive correlation measures increase OR decrease together Correlation 5 causation Causality T Relation of cause and effect can conclude experimental manipulation has specifically caused result Can t know causality with correlational study Levels of analysis Scope of experimental approaches need to use levels that are just simple enough Social interaction organs neural systems brain region circuit level cellular level synaptic level molecular level LECTURES 42 48 AND CHAPTER 2 fMRl functional magnetic resonance imaging PET positron emission tomography detects changes in blood ow and identifies brain regions that are active during task 0 can show how networks in brain interact 0 high spatial res low temporal uses tomography and injections of radioactive substances used by brain in order to view functioning 0 Measures blood ow if brain area being used blood will ow to that area 0 High special res low temporal EEG L electroencephalography MEG magnetoencephalography neurons generate small electric fields measure activity on surface Smaller time scale high temporal res low spatial measure magnetic fields of neurons High temporal res low spatial Spatial resolution L Temporal resolution L WHERE in brain 0 fMRl PET WHEN in brain 0 EEG MEG Limits of specific techniques fMRl amp PET versus EEG amp MEG L Limits of neuroimaging in general fMRIPET high spatial low temporal res Takes picture every 2 seconds Only measures blood not neural activity EEGMEG high temporal low spatial Only measures activity on surface Always sacrifice one for the other temporal spatial Correlational not causational Data hard to interpret Causal inference L Can correlate a cause with an effect 0 TMS patient brain damage animal studies Patient studies L Brain damage impairs specific behaviors What can patients do not do beforeafter damage Limits no 2 lesions in same area consequences affect behavior TMS Transcranial magnetic stimulation general technique and proscons applies magnetic fields to stimulate cortical neurons to identify discrete brain areas that activate during behavior 0 Used on healthy people Create reversible virtual lesions Interferes w brain s electrical signals Helps prove localization of function Limits locality assumption no network effects OOOO Optogenetics L Animal studies pros and cons L Optogenetics animal study manipulate activity of subsets of neurons high spatial and temporal res Pros can correlate cause with effect Limits subjects aren t human Neurons Unit of nervous system composed of receptive extensions dendrites integrating cell body conducting axon transmitting axon terminals cg 143 5NV lgt Igt quotxf1l2re39iKlgt F n R J 0m I ou39ta m r may I 7 Kg jlial cells Nonneuronal brain cells that give brain structural nutritional etc support Relative and approximate numbers of neurons amp glia in brain L 85 billion neurons 85 billion 4 trillion glia Dendrites Extension from cell body that receives info from other neurons Cell bodySoma Region of neuron w cell nucleus Axon Extension from neuron that carries action potentials from cell body toward axon terminals Axon hillock Integration zone axon hillock combines info from dendrites to determine whether to send own signal Axon terminals End of axon that forms synapse on neurontarget cell transmits presynaptic cell s signals across synapses to postsynaptic cells Sensory neurons T Motor neurons T lnterneurons T Directly affected by changes in environment light odor touch Transmits neural messages to muscles or glands large in size Most neurons in brain are of this type receive input and send output to other neurons small in size Multipolar neurons Bipolar neurons Unipolar neurons Presynaptic membrane Postsynaptic membrane 39 v5 Many dendrites and single axon Y f quot M5 c cccc 7ltwquotlt F N Pltgt quot W 35 C o m M01 ivi Ii xmx 7A w E 1 dendrite at one end one axon at other common in sensory systems vision I Cvquot ilquotif branch that leaves cell body and goes in 2 directions one end input one end output D sui K Po 1quot AX k mvx region of synapse that releases neurotransmitter region of synapse that receives and responds to NT Synaptic cleft Synapse Synaptic vesicles space between presynaptic and postsynaptic neurons at the synapse small structures in presynaptic axon terminals that contain NT molecules Neurotransmitter Chemical released from presynaptic axon terminal that is basis of communication btwn neurons Receptors Protein that captures and reacts to molecules of NT hormone o Alter excitation of post synaptic neuron 0 Makes moreless likely to release own NT Type of glial cell forms myelin in CNS legs spread to many Oligodendrocytes axons Schwann cells Type of glial cell forms myelin in PNS whole celll myelin sheath segment Myelin Multiple sclerosis T Fat insulation around axon formed by glial cells Improves speed of conduction on axon Disorder where myelin degenerates Nodes of Ranvier Gap btwn segments of myelin sheath where axon membrane is exposed APs jump between nodes Astrocytes Star shaped gl1al cellw1th many extensions running in all directions Bridge between blood vessels and neurons Microglia Small glia that remove cellular debris from injureddead cells Central nervous system T Peripheral nervous system T NOT cranial or spinal nerves CNS includes brain and spinal cord PNS includes all nerves and neurons outside brain spinal cord Nerves versus tracts Ganglia versus nuclei Nerves axons in PNS Tracts axons in CNS Ganglia cell bodies in PNS Nuclei cell bodies in CNS Autonomic nervous system T Sympathetic versus parasympathetic nervous systems T ONLY to the extent of the three text boxes in Figure 29 page 33 Consists of the sympathetic and parasympathetic NS SNS fight ight o prepares body for immediate action 0 Ex blood pressure raise pupils dilate HR up PNS restdigest o helps body relax recuperate prepare for future action 0 ex BP lowers blood vessels relax HR down digestion stimulated Cerebral cortex Outer covering of hemispheres consists mostly of nerve cell bodies 0 Higher brain function Gyrigyrus versus sulcisulcus Four lobes of cortex Corpus callosum Three planes of orientations see Box 22 page 35 T Directions dorsalventral rostral caudal T Brain terrain bumps are gyri grooves are sulci Frontal parietal occipital temporal lobes x s 3 Q39 lt quot l W 439a ampltI PO tfi I 4 I 9 l 54 W Z f L 39 Q P fquotfl v quotif i R M F 0 f L Lt I vs p8Q Q I 39 39 A I P yP hr J9 lQ H pnq g 11 C quot gt V U pig nO 1 Main band of axons white myelin connecting 2 cerebral hemispheres I I 5 Horizontal iLlI 7quot 39o 39Ir l r r r I q 39 IquotI39o39In bagnttal E White matter vs gray matter Developmental divisions of the central nervous system Figure 212b White matter primarily myelinated axons Gray matter primarily cell bodies Layers of cerebral cortex Figure 213 p38 Six layers Visible with staining Basal ganglia Group of forebrain nuclei candate nucleus globus palidus putamen deep in hemispheres o Specializes in habitual movement riding bike driving car tying shoes Amygdala Hippocampus Thalamus Hypothalamus I Frontal lobe Part of the limbic system 0 Emotion odor Tmlamus Learningmemory Part of diencephalon Sexaggression hormones Amygdala Midbrain Substantia Nigra Parkinson s Disease L Relay system for Visual Hpomaam auditory motor 2 Midbrain structure L O ctoy bu Reward add1ct1on mvmt quotquot Dopaminergic neurons Death of dopamine neurons in SN cerebellum Hindbrain structure Balance fine motor Menmges Brain protection dura matter arachnoid pia matter Cerebrospinal uid Ventricles general purpose not specific location of each T CSF lls cerebral Vesicles part of brain protection circulates around brain Produce CSF by ltering blood Bloodbrain barrier Regulates What gets access to the brain Junctions of cells line blood Vessels and astrocytes LECTURES 49 414 AND CHAPTER 3 Polarization Depolarize LESS polarized charge closer to zero than starting point generally more for neurons Hyperpolarize MORE polarized charge further from zero generally more for neurons Ions Resting potential Charged atoms Basis of action potentials in neurons Affected by forces diffusion and electric 60mV inactive net movement of ions is zero 7 5 3 7 mot1amp1 1 r Ion channel Potassium ions K On the cell membrane of a neuron let in particular ions and keep others out Can be voltage gated leak Potassium w positive charge In cell at rest K is mostly inside the cell drawn to negative membrane potential of cell Diffusion Concentration Diffusion gradient L Electrostatic pressure Electrical gradient Ions move from greater to lesser concentration Na Wants to get IN the cell because more outside than in Positive ions attract to negative ions like charges repel Sodiumpotassium pumps Sodium ions Na Bring K IN to cell push Na OUT of cell Return cell to resting state At rest concentrated OUTSIDE cell At threshold come in through presynaptic ionotropic channels Voltage gated Na channels open at 40mV Na rushes into cell to cause AP Equilibrium potential NCI IIIOVCIIICIII OI 1OI1 III qL1CSt1OI1 1S ZCI39O Threshold Action potential detailed steps eg Figure 36 and lecture on 410 0 l 39 l f x 1 1 N5 Na ions from presynaptic cell s AP diffuse into axon hillnnlz at AlmV THRPQHQI T3 Na nhnnnelq npe11 Reversal in membrane potential caused by Na ions opening voltage Na channels and Na rushing into cell then Na channels close and returns to resting potential I z9t wlt2 i 5 391 1 squot 39 C quotl l K 139 s N3quot v0 QW3 M 03 quot l at V D 1 O C O N 675 1 5 sg 0 ac Q Q0 P Allornone property T Voltagegated Na channel Voltagegated K channel Analogy ushing toilet o No matter how hard you push on toilet handle ush won t be any bigger or more powerful but ushes will happen more often No matter how much stimulation is applied to a neuron AP will not be any larger in amplitude only more frequent or less freouent Closed at rest opens at threshold 40mV closes at peak of AP 40mV Closed at rest opens at peak of AP 40mV closes at rest Refractory phase T Period of time where AP cannot occur channels won t reopen so AP can t go up the cell backwards Saltatory conduction Al Jumps along nodes or Fanvier llnltiple Qrlernqiq T Neurotransmitter Presynaptic vs postsynaptic cells Myelin degenerates Chemical released from presynaptic axon terminal that serves as basis for neural communication 0 Ex donamine Ach Presyn cell that sends NT Postsvn cell that receives NT signal Postsynaptic potential potential that occurs because of IPSP or EPSP in postsyn cell Chloride ions Cl IPSP inhibits AP makes less likely by releasing Cl ions and making cell MORE negative away from zero thus preventing AP EPSP makes AP more likely because Na ions make cell more positive more likely to reach threshold Released because of IPSP to prevent AP Spatial summation Temporal summation Lots of neurons close by add up to make AP Neurons fire in quick succession if happen at same time more likely to combine to threshold Synaptic transmission Synaptic vesicles Synaptic cleft aka synaptic gap Calcium ions Ca2 U 39gtquot sodium diffuses down axon terminal from AP calcium channels open to let in positive ions calcium makes synaptic vesicles sticky and move vesicles attach to synaptic membrane and open NTs released from vesicles into synaptic cleft NTs press on ionotropic or metabotropic receptors on postsynaptic cell NTs degenerated and or reuptake occurs Spherical structures inside axon terminals that hold NTs Space btwn postsyn and presyn cell Released when sodium diffused and make cell more positive Ligand Receptors Protein that binds to receptor N39l Ionotropic let ions in when NT binds SHORT TERM Metabotropic change structure of cell when NT binds LONG TERM Agonist Helps or mimics particular NT Antagonist Decreases productivity of NT UCg1 aClaU011 Enzymes break down NTs in synaptic cleft Reuplake Transporter cells take NTs from synaptic cleft back into presynaptic axon terminal Transporters Take NTs from cleft to presynaptic cell Types of synaptic connections T see gure 313 Dendrodendritic Axoaxonic Axodendritic Axosomatic Epilepsy T Seizures T Too much glutamate in brain electrical signals re rapidly Mapping the human brain T Figure 317 LECTURES 415 417 AND CHAPTER 4 Exogenous T Endogenous T Originates outside body drugs opiates Originates inside body released after pain endorphins Ionotropic receptor Metabotropic receptor Discovery of acetylcholine see Fig 43 Acetylcholine Basal forebrain receptor that can let in ions such as sodium but NTs do not enter receptor that cannot let in ions NTs do not enter but NTs can cause long term changes in the structure of the cell Otto Loewi frog heart experiment Had two frog hearts stimulated first heart with electricity and took surrounding liquid of heart 1 out and put liquid into second heart and second heart contracted like rst heart Proved that neurons communicate chemically Sent from basal forebrain sent to the cortex amygdala hippocampus PNS major role in CNS is learning and memory modulation major role in PNS is parasympathetic activity where Ach is sent from Dopamine Ventral tegmental area VTA sent from midbrain VTA and SN sent to frontal cortex basal ganglia nucleus accumbens Major roles reward learning motivation conditioning popular NT for abused drugs Parkinson s disease is de ciency in dopamine schizophrenia is too much dopamine sends dopamine how it gets to rest of brain Glutamate sent from everywhere and to everywhere most dominant excitatory NT too much glutamate causes seizures sent to and from everywhere most dominant inhibitory NT GABA alcohol GABA agonist I 198 d any protein that binds to receptor NT or drugs Agonist increases paIquot1CulaI lJ 1 activity Antagonist decreases particular NT activity Metabolic tolerance T Functional tolerance T Downregulate T Upregulate T body gets better at breaking down a drug metabolism gets faster body makes more upregulation or less downregulation receptors for certain drug decrease the number of available receptors for a drug increase the number of available receptors for a drug Drug effects on transmitter production transmitter release transmitter clearance receptor activity postsynaptic activity understand general mechanisms of how drugs can affect each stage and how a drug could be an agonist or antagonist at each stage Neuroleptics Antipsychotics ex amphetamines are dopamine agonist increases amount of dopamine can increase amount of NT released agonist reuptake and degradation can block receptors increase receptors pretend to be drug IPSP or EPSP more or less likely to cause AP block dopamine receptors ex alleviate positive symptoms of schizophrenia eg hallucinations atypical antipsychotics block serotonin receptors Monoamine oxidase MAO inhibitors Selective serotonin reuptake inhibitors S SRls old antidepressants block the enzymes that break down certain NTs so NT stays in synapse for longer AGONIST for NTs antidepressant inhibit reuptake of serotonin leave serotonin in synapse AGONIST for serotonin Benzodiazepines antianxiety valium activate gaba receptors inhibit neural activity Morphine Heroin Endogenous opioids Nicotine major active substance in opium powerful pain killer analgesic artificially modified potent form of morphine increases dopamine opiates meant to work like endorphins which are body s natural pain killers internal substances released in the body for pain relief pnrln1hl1inQ agonist on cholinergic Ach receptors stimulant stimulates and then depresses neural activity enhances Alcohol GABA to inhibit neural activity THC major active ingredient in marijuana Endocannabinoid endogenous ligand of cannabinoid receptors marijuana produced bv brain anandamine for example Caffeine inhibits inhibition antagonist for adenosine Adenosine blocks dopamine and glutamate So caffeine increases dopamine and glutamate pocalne enharlces catecholarrlirie I1euroLraI1sII1issioI1 SLlIIlLll39clIlL blocks reuptake of monoamine from synapses blocks reuptake of dopamine and produces more dopamine release Amphetamine resembles structure of catecholamine transmitters and enhances their activity builds up dopamine and norepinephrine by not breaking down and by transmitting LSD increases serotonin activity in visual cortex has powerful hallucinations and spiritual feelings MDMA ecstasy derivative of LSD stimulates visual cortex OLIVER SACKS CHAPTERS Chapter 2 The Lost Mariner Chapter 10 Witty Ticcy Ray Chapter 18 The Dog Beneath the Skin Man only remembers things before 1945 short term memory loss Tourette s syndrome Smell enhanced for brief period of time
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'