Brain and Behavior-Study Guide-Exam 2
Brain and Behavior-Study Guide-Exam 2 Psyc 300
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This 14 page Study Guide was uploaded by AlexaR. on Wednesday September 16, 2015. The Study Guide belongs to Psyc 300 at Northern Illinois University taught by in Spring 2015. Since its upload, it has received 147 views. For similar materials see Brain and Behavior in Psychlogy at Northern Illinois University.
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Date Created: 09/16/15
gr Chap 5 Synapse Chemical Si tnal Suggested byl tto391quotLoer that neuronal communication is chemical signals He wanted to test if chemical signals were an important part of Central Nervous System He had a dream of how to experiment this Used frogs heart in a jar39connected to vagus nerve He stimulated it to change the beating of heart and recorded ltquotquot s owed the rate of firingbeating He ii tran sfers the jars fluid to another heart that wasn t simulated The rate also slowed He found thatacetylcholineneurotransmitter was in the fluid Acetylcholine causes cardiac tissue to relax but skeletal muscles to 39 contract neurotransmitters have different effects depending on the target Stimulating accelerator nerve led to the discovery of epinephrine 39 Epinephrine increases heart rate This led to many other experiments Anatomy of tha Syna Axon Presynaptic Terminal terminal button Synaptic drift Dendritic Spine Dendrite n J Vs 1 IQEiQi Synaptic Connection how do we distinguish excitatoryinhibitory when looking through a microscope 2 If W5 27 39 if r 39 xx quotIJ J 4quotquot7 EEchtatory Usually located on dendrites Presynapticgjiggg 31 VesiCIes Wide cle it has to diffuse around this Postsynapticidenggr active zone lnhibitory Located on some cell body or axon F Iatter vesicles Narrow cleft Postsynaptic Looking at this we can see how cell is receiving info Always a battle between excitatory and inhibitory in dendrites it39s an equal amount of excitatory versus inhibitory w Ltjf ELchations as we get closer to cell body or axon it is closer to one side Each step decides if the action potential will continue Den 1rodendriticWhere two dendrites come together Has39ilittl e influence on membrane pctential 39Axotjeridritic axon synapsing on dendrite Over a small area can b iexcitatory u or inhibitory Axoz eX tr aicellular releases neurotransmitterthat can change potential or multiple synapses Has a larger effect can be inhibitory or excitatory 39 tends to be more inhibitory tifogsynaptic another axon synapsing from another neuron39onto an axon 7 Inhibitory I 4 i 1 l J sw we r f39 k i P iqusegretory can haveWide Scale effects across body of CNS Excitatory or Inhibitory last point the action potential can be turned off Inhibitory lnformation can be processed without getting out such as not acting out a dream A 39la39 1 39 r235 as a 7 Ni39ei 39lii li Ti a ii ibeGetting signal from neuron to neuron making neurotransmitters 1 39 nthesisgf activation of tom RNA to Proteins but this takes longer Endorphin painkillers are made this way Others like acetylcholine are made in 7 Doesn t involve activation of DNA 2 Storaf eij Even if you39re involving precursor chemicals it needs to be stored so it can have controlledrelease Some drugs can change how well they re stored 32 Release Wood an action potential traveling down membrane Opens calcium channels oaICi39um binds with calmod lin this forms a complex The complex binds with vesicles Calmodulin allows the NT to be released from microtubules The vesicles clock in presynaptic terminal Opens into synaptic cleft w V Thei39neurotransmitter can be released 4T Receptor Activation can include many different things Neurotransmitter will bind to channel can open it up or activate many things including DNA orjust ISPS Neurotransmitters can change as you age Ex EPSP becoming IPSP There are also pre synaptic receptors for feedback binding deactivate neurotransmitterquotfrom synaptic cleft turningdo gthie a Diffusionfdiffuses away on it s own higher to lower concentra on Enzyme BreaksNT apart into simpler units that won t activate receptors Some parts can be used then other diffuse Acetylcholine uses this c Reuptak f NT is reabSprbed presynaptically Clears out synapse so next signal can be read Dopamine uses this 1 Glia C ilf 4astro39cyte Carr absorb components being releasedgait Asynapseand providethem back to the neuron Neurotransmitters algefhtilicatilon how do we know we are dealing with a NT P f iSynthesisz how it s made Chemical must be present and made Release Show that there s controlled release trEffect on Target it does something to system Deactivation we can turn it off once it s released Small molecule can be made on sitesynapse ex Dopamine serotonin GABA 7Fast acting Obtained from diet quotdon t involve activating DNA Can be precursorbiochemical pathway quotquot Ex Tyrosine hydroxylase L Dopa DopamineeNorepinephrin epinephrine Can be rate limiting factors that increase or decrease amounts Ex Focus on Disorders Awakeningsmovie with neuroscientist Oliver Sach i iParkinson s disease degenerates substancia nigra LDopa low dopamine loss of movement or can t turn movement off can treat with dopamine but can develop tolerance and cause schizophrenia symptoms t39te ncephalitisilnfection of CNS quotTargets substatia nigra Physical activity has been found to slow progression of disease Peptidesex Met encephalin leu encephalin Slow acting Slow replacement Ti mad e 39in nucle usi have to activate DNA Ex People with chronic pain it can block it at rst but once you use it up it can t keep up More needs to be produced LQReceptors Three classes 1F3 t 6notrobic receptors Directly connected to ion channel NT will bind open and let ions in Rapid changeS quickly produce IPSP or EPSP N o lasting effects on function of neuron Can quickly change direction of pencil Change train of thought Metabotro I39on channel Coupled NT binds to receptor 6 protein opens ion channel Slower changes in membrane potential Short term effects Could be left open for longer could impact neuron for minutes Change in arousal after a scary movie Enzyme coupled high plasticity but a finite amount 39 G protein activates enzyme Enzyme messenger Slower changes 39 Lasting effects on function Can be lifelong lncludes memory Have to make sure you don t get memory confused with motor control such as fatigued muscles How to tell the difference Action potentials are still generated SynaptngearnLgr Changes in neurons support this Forms y39ssociative learning you havei i tieraction With stimulus and incmase or decrease 5 in reactivity showidecreas39e39 in reactivity to stimulus that s continually presented 1Sensitization show increased responsiveness to continued stimulation Ex Watching a scary movie then hearing rustle and freaking out K ande l39 Nobel 2000 studied this memory occurs at synapse great changes to support this used aplasia snail has huge neurons and simple network of neronsi Shocked him in siphon so he has reflex which shows learning the longer its contracted because he has learned the world is a dangerous plate if the siphgiin is only contracted for a short time he has not learned Habituation39 Behavior Squirt water and gill contractsi observe how long 39ll quot you continue the gill will remain mirage Neurons Siphon sensory Gill motor Synaps e changes occur fDecreased C32 influx Less NT released Before habituation calcium channels open bind to vesicles and create release After habituationquot less calcium isi in less binding to vesiclesquotless N T release less EPSFquot less tendency to contract gill shorter term Fehavio Mild shock to aplasia s butt nowihe is more responsive to stimulation of r je t like a bird biting him he is feeling in danger Gill has become hyper responsiVe and contracts all thetime fNeu rons Siphon sa sensory Feels shock Tail interneuron Process feeling NGill motor Causes to retract Synapse quotSerotoninquot released by interneuron reduced potassium ef ux Prolonged action pote39ntialbecause of potassium channels 39potassium channels close can39t leave neuron Prolionged action potential results infmore calcium influxand I yesicles docking so increased transmitter release greater EPSP g causing greater depolariilition of presynaptic membrane Na ff 4 5 ex More likely to see gil contract Long Term Memory Structural change synapses are lost or added to support long term memory Chapter 6 Drugs and Behavior 39 H Drug Action 7 ways drugs can change neurotransmitters Leiawear dmihis tratioh how the drug enters CNS 39fOra39feasiest l safeSt39 and most convenient but digestive limitations can lead to breakdown TcpicafL absorbed through skin and intro bloodstream Can cause skin irritation Intramuscular inject into muscles diffuse into capillaries Inhalatfdn immediate access to CNS but can result in infection lntravenousdirectly into circulatory system rapid effect Raises chance for infection even more Intracerebral injected directly into brain Not used often only for infection because antibiotics can t cross blood brain barrier Blood brain barrier is an obstacle for oral topical intramuscular things that can prevent drugs from working can also prevent infection Each route changes how the drug works temporal characteristics ex Cocaine tlntravenous quick peak in concentration of drug after injecting that gradually decreases lntranasal no rapid peak effect is a bit lower but a bit longer lasting Ora39l spread over tie diffuse increase and decrease LQtBlood Brain Barrier areas the blood brain barrier is weak Pituitary entry of chemicals influence pituitary hormones stress regulation Pineal gland entry of chemicals that regulate daynight cycles quotArea Postrema toxic substances that induce vomiting Synaps e a drug can effect multiple NT in multiple ways AFAgoniSt any substance thatffacilitates neUrotransmission BT39Anfagoniist substance that fprevents neurotransmission in 1 Synthesis drugs can increase number of precursors agonist Or vesicles can be released more frequently agonist 2 Storage drugs can cause vesicles to become leaky releasing and breaking down NT antagonist Or vesicles can be released more frequently agonist 3 Release drugs can stimulate release agonist 4 Receptor Activation drugs can bind to receptor and act as NT agonist Or can bind preventing NT from binding antagonist 5 Inactivation drugs can prevent inactivation agonist Or facilitate inactivation antagonist 6 Reuptake drugs can block reabsorbtion antagonist There are many points drug companies can manufacture drugs to target exrACetylcholine a synthesis viet how precursors are obtained Egg yolks olive oil agonists release ibla ck widow spider venomf Rapid release paralyzed you andgggitease heartrate agonist 39t treCeptor activatibn nicotine sits in channels remaining open agonist 39 curare binds to receptor and does nothing Paralysis Acetylcholineo n t bind now and have effect antagonist t inactivation sarin gasused in certain weapons Causes permanent inactivation of enzymeacetocholinestarase that breaks down acetylcholine Now it39s just dumped into synapSe Rigid paralysis and heart rate decrease agonist ariceptquot used to treat Alzheimer s where you have lower acetylcholine Temporarily binds to acetylcholinesterase to allow levels to increase in synapse agonist Ex Dopamine movement and reward 39 synthesis L Dopa increases precursor reuptake cocaine amp amphetamine block the reuptake of dopamine agonist release amphetamine promotes release of dopamine agonist receptor ichlorpromazine occupies the dopamine site on the D2 receptor preventing receptor activation antagonist Classificationnot only based on shape mostly based on behavioral effects agitAntianxietv agents and sedative hypnotics sedative ex alcohol barbituratesibefore surgery Anxiolytics ex quotvalium diazepam after stressful situation Uses calming someone down Sedation anxiety reduction quot S ite of actionquot tGABA inhibitory NT IPSP receptor GABA allows chloride to flow in negative charge hyperpolarize lPSflf quot sedative hypnoticscan open channel by itself or bindn themselves to ioih channel to open up is iantianxiety site Where benzodiazepine binds it helps GABA find for longer IF GABA doesn t gind benzo doesn t work or open channel If you mix these you can die because too much chloride is flowing in and shutting down all action potentials because gaba IS in the medulla oblongotta for breathing and heartrate ECQmplications Fetal Alcohol Syndrome Tolerance stress tol era n o39e can lead to tolerance of other drugs I Coma Abuse potential br ntipsvchotic agents ex Chloropromazine 5 Haloperidol 39 Uses schizophrenia Theres been a reduction in number of mental patients in hospitals but where are they going quotSite of actidn Dopamine receptor it blocks NT by sitting on D2 receptor Amphetamine and cocaine Not an increased number of dopamine receptors or dopamine so other receptors are involved TComplications7 quotParkinsns type dyskinesia since we re blocking NT reuptak e c LQJAntidepressants 6 of adults suffer from depression ex Prozac Zoloft paxil Uses Major depression thought of suicide prolonged feeling of guilt worthlessness OCD reoccurring thoughts compulsive behavior checking Site of action seratinergic system MA O inhibitors prevent breakdown of serotonin SSRl prevent reabsorbtion of serotonin Stay in synaptic cleft longer take 2 or more weeks to become effective even though they work at synapse right away T Complications MAO can have lethal food interactions like cheese N rcdtic analgesics agonist ex iMm Phine Heroin Use 3quot pain re d uctioriiw tSleep in high doses Site of action fenddgenous opioid receptors occupy this site fComplications Supress respirationheanrate High abuse potential EX G Ence Emergence t fDecrease in a drug s effectiveness over subsequent administratio Alcohol prisoners given alcohol for 13 weeks enough to keep them gintoxicated l subjects increased their intake After 15 20 days of consumption the signs of intoxication and blood alcohol levels fell P otential Factorsin tolerance effectiveness Change in liver metabolism quot Change in neuro ns formation of silent receptors to bind to alcohol and have no effect v39 Learning classical conditioning Classical Conditioning T Stimulus quotReflexi Us food yU S39FEUR 7 Response Toneno drooling UR drooling CS NR CS Tone NR no drool USCS UR both paired CS CR drooling with done alone jquot39 quot39lquotJZ E Fl39lItorph i39n e narootic UR quotanalgesisadegreased sensitivity to pain 39C S f environmental cues location CR compensatory response physiological response that changes UR LQ Siegle studied tolerance and overdoses Stories that people OD and still have amount of drug in needle Found that people who OD were in an environment they never used before Body doesn39t prepare for a new environment Develop assessment of pain for rate hot padslicking paw give morphine take longer to lick paw two contextszquiet hot plate room and loud home cate M Hot 8 Hot M Cage M Hot developed tolerance saline stayed the same when M cage was put in new context they were not tolerant Compensatory Response CS conditioned stimulus present US unconditioned stimulus absent Give rats morphine and they build tolerance Just give them environmental cues and they have fiingreagsed sensitivieylirritability Cues withdrawal symptoms Extinction of CR 2 groups were given same amount of morphine MPM group returns to plate and gets a saline placebo M Rest group stays in cage 2 week break then given equal morphine to both CID 5 th lacebo mad the morphine more effectivequot Practice Exams 1 EDegradation is the deactivation of an MT in the synaptic cleft by enzymes 2 Wietyldholine has been related to Alzheimer s 3 Nitric oxide is a gas NT that dilates blood vessels in active areas 45 Parkinson s disease is linked with a loss of dopaminein the midbrain 5 In the mammalian brainfGABA is main inhibitory NT and glutamate is main excitatory NT 6 In AwakeningsLDopa was used to treat patients with rare movement disorders that followed flu outbreak in 1920 s 7 eDifosion is the process of NT deactivation whereby the simply leaves the synaptic cleft 8 rsynaptic cleft is the space between an axon terminal and a dendrite 9 A drug that reduces do pamine release at a synapse is an example of an antagonist 10 Tolerance is a decreased response to a drug over time 11 A drug that blocks the release of acetylcholine is called an antagonistquot 12 A drug that prevents breakdown at synapse is an agonistf 13 Selective serotonin reuptake blockers are used in thetreatment of depresslojni 14 Order from least to most efficient method of administration ioral consumption inhalation injection into bloodstream 15SSRl s treat depression by blocking the reuptake of serotonin 16 It is suggested that high levels of stress can damage neurons in the hippocampus
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