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146 Cards in this Set
- Front
- Back
major depression |
unipolar depression characterized by extreme low lasting a few weeks-few months if untreated |
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1.interacting genes |
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genes that increase depression risk for each syndrome |
1.early onset:b4 30yo:have relative w anxiety,depression,adhd,alcohol,bulimia,migraines,ocd,weed addiction&irritable bowel syndrome) |
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borbona disease |
viral infection found in 1/3 of ppl with depression&schizophrenia.infection in farm animals cause alternating frantic&inactive states |
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*4 hormones in women *1 in men *2 in both |
W:1.estrodiol&orifesterol cause new symptoms 2.high cortisol(stress hormone)late in pregnancy &early in morning:after birth,20% get postpartum depressed.overian horm. change to deliver 5.catecholamines:dopamine&norepinephrine |
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have more stable activity in prefrontal right cortex regardless of symptoms.causes change in synapses to nucleus accumbens which make it unresponsive to reward. |
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1/2 of teens w insomnia get depressed in 6yrs. |
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typical antidepressants work |
vary in targeted nts but all increase BDNF&seretonin nts release |
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*catechomines in depression |
dont release seretonin:inhibit catechomine(dopamine&norepinephrine) reuptake. |
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treat depression:block transporter protein that reabsorb serotonin&catecholamines into presynaptic neuron after release to prolong nts presence in synaptic cleft&stimulate postsynaptic cell. |
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1.SNRI:block serotonin &norepinephrine reuptake |
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MAOI:no food w tyramine(cheese,raisin)b/c combo increase blood pressure.block presynaptic terminal enzyme MAO(break/metabolize catecholamine&serotonin into inactive form)so presynaptic terminal can release more. |
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cons:herb isnt regulated&purity varies by bottle. |
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*relation to how brain stimulation treatment works |
work well(esp if young).limit:depression rating scale isnt reliable at low level depression
*brain stimulation treatment works 50% of the time if others fail:after many months&repeated treatments |
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*retrograde amnesia |
1.ECT&repetitive transcranial magnetic stimulate:new neuron proliferation&alter 120+gene expression in hippocampus&frontal cortex.cause retrograde amnesia |
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bipolar disorder:prevalence, gender/age vulnerability |
manic depressive disorder:1%of ppl w onset in early 20s.both genders can get it but men get BP1 b/c women get help.link w many genes&disorders as well as sleep deprivation |
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the 3 episodes/2 bipolar disorder types |
depression is paired w 1 other episode type |
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*people alternate b/w 2 poles:mania:brain increase &A receptor(which increases glutamate&glucose) |
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most common&1st bipolar treatment found by JF Cade(thought uric acid relieve bp disorder).mix uric acid(urine component) w lithium salt to help it disolve.stabilizes mood,stop relapse.regulated b/c high dose is toxic |
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valproate(depakote)&carbamazepine less effective but treat bipolar disorder.pair w antidepressant |
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1. decrease AMPA receptor # to decrease glutamate. |
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why seafood helps treat bipolar disorder |
counter acts arachidonic acid synthesis b/c it is an omega 3 polyunsaturated fatty acid |
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seasonal affective disorder:what is it,where it is seen&treatment(how it works) |
SAD:less severe depression in 1 season prevelant near poles. treat w bright lights w benefits seen in 1 week.light affect serotonin synapses&alter circadian rhythm |
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sleep pattern of depressed/bipolar vs someone with SAD:possible cause |
depressed/bipolar have insomnia&wake early. ppl w SAD have phase delayed sleep&temperature rhymes(sleepy/wakeful later than avr).ppl w SAD have mutated gene responsible for regulating circadian rhyme |
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brain stem:what it does&1 structure it contains(&its function) |
processes salient(a strong/noticeable) event. |
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function of the corpus callosum&what it is |
bundle of fibers responsible for communication b/w hemispheres |
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processing emotion:what it consists of |
2 independent processes join for a double process.evidence in facial paresis |
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autonomic nervous system:2 branches |
involved in different combo for all situations. |
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sympathetic autonomic nervous system:role in fear |
hypothalamus causes fear(<3&blood rate increase)which leads to panic attack if extreme arousal.ppl that detect their autonomic response consciously identify danger. |
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symptom/response:feel less intense/no emotion but claim to empathize. |
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theories of emotion:according to 3 components of emotion |
after you perceive a stimulus: |
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james lange opinion on emotion
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emotion are embodied&used to label experience.ex. you run b/c you're afraid |
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walter cannon discovery related to autonomic nervous system |
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emotion components:issue w theory |
1.action impulse:physical response. |
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emotions as motivations:explanation&issues |
internal processes modify response to an external stimuli class.issue:joy,fear,sad aren't motivations |
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emotion is all over brain.can identify whether an emotion is -ve or+ve but not specific emotions |
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forebrain area around thalamus is critical for emotions |
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insular cortex:location,what it interprets&damage |
in primary taste cortex.activated in different parts by different types of disgusting images/expression(& a bit by fear/anger).cant feel disgust if damaged |
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evidence against james lange *method acting |
*can feel emotions to same degree but can't express them: 1.Mobius Syndrome:cant smile/move facial muscles. *method acting:make self feel emotion to show natural reaction |
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amygdala:3 roles(when it works best) |
1.detect/mirror unpleasant stimuli(fear,disgust& anger not sad,joy)&pleasant w focus.best if attend eye&averted gaze(more energy/active if ambiguous hard to read face). |
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amygdala w high response linked to 2 things |
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1.cant rate,draw®ister emotional stimuli(include surprise)b/c dont attend eyes.*SM find uncomfortable stuff to be comfortable |
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escape behavior:what amygdala axon does |
axon send input from pain,vision,hearing down 1 of 2 paths to cause |
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pathway for conditioned fear:3 parts |
circuitry |
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take 0.2seconds: 1.amygdala axon |
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attack behavior |
anger&aggression:increase w |
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#1.low cortisol:low fear. |
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5HIAA is a metabolite found blood,cerebrospinal fluid&urine thats used to infer turnover rate for serotonin(amount neuron release,resynthesize&replace nts).cerebrospinal fluid is best measure.*low 5HIAA means low serotonin. |
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tryptophan influence on men |
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ratio b/w index &ring finger shows testostrone levels from utero (used to stop miscarriages) |
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prefrontal cortex role in attention&memory |
*get input from dorsomedial thalamus. |
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damaged prefrontal cortex:4 impact on decision making/ emotion |
lesion&kid:1.make impulsive/irrational choice wout consequence thought for fast reward |
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4 moral dilemmas:how ppl w damaged amygdala,prefrontal cortex &cingulate gyrus respond |
if choice b/w killing 1 person&saving 5,they use logic(utilitarian)&save 5.normal ppl rely on emotion:trolley(pull lever kill 1).footbridge(push fat guy off bridge), lifeboat (sinking boat,push fat guy off), hospital(kill healthy man for organs) |
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ioga gamble experiment:who studied it *results |
*ppl w prefrontal lobe damage show no skin response b4 picking a 'bad' card deck A&B:high return&loss-more risky so bad choice
Deck C&D:low return&loss:not risky so good |
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frontal/temporal lobe/cortices activity |
1.important for wide emotion range. |
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behavioral activation system |
BAS:left hemisphere has low-moderate arousal.approach(fight).high prefrontal activity:happy,outgoing,fun love |
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BIS:right hemisphere.more attention&arousal.Stimulate&more response/detection to emotion stimuli(fear&disgust:avoidant:flight response).frontal activity:socially withdraw,unsatisfied&prone to -ve emotion.damage:cant identify emotion:recall -ve memory wout -ve emotion |
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anxiety:amygdala(not always abnormal)&hypothalamus. |
in teens&Women |
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chl in panic disorder |
GABAa center has chl channel surrounded w 4 units w 1+ sites sensitive to GABA.alchohol help Chl flow so drug blocking alcohol effect block behavior issue. |
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no drug target.block learned fear/avoid behaviour: |
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Benzodiasepine for anxiety:how it works, side effects, result |
bind w GABAa receptor&sites on 3/4 unit.twist it so GABA bind&increase for less anxiety(include midbrain.inject into amygdala:relax muscle&increase social approaches to other).not lasting solution.Side effect(addiction, fatigue,block epileptic convulsion&impair memory)in thalamus&cerebral cortex. |
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interfere w protein synthesis at some amygdala synapse&blocks fear reconsolidation.extinguish trauma if kid&new.slow exposure suppresses(not eliminate) 1st learning in adult |
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David Chalmers |
came up w 2 problems |
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Mind-Brain Relationship |
no mental activity wout brain activity.the biological explanation(ex.feel happy b/c dopamine increase)raise issue. 1.Dualism:rene descartes:mind&body are independent substance kinds that interact at the pineal gland(smallest unpaired structure he found). 2.monoism:universe made w 1 substance kind |
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3 categories of monoism |
1.materialism:all that exists is material/physical&psychalogical experiments are explained w physical terms. |
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gamma wave(travel at 30-50hz frequency)activity synchronize(increases summation opportunity)&spread from V1(active if unaware& aware)to other brain areas(prominent cluster activation in superior parietal&dorsolateral prefrontal cortex)for conscious awareness |
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consciousness according to psychology |
cooperative ppl report a stimulus that theyre aware of |
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Binocular Rivalry |
brain switches focus b/w different images sent by each eye individually.occurs roughly every 2 seconds on avr |
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something complex in scene changes slowly/when you blink&you dont notice&are unaware of obj in full view |
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bottom up attention |
Bottom-up attention:Reaction to stimulus |
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what type of phenomenon is consciousness&why |
a yes-no phenomenon b/c you can't be unaware&aware at the same time |
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what broccoli increases what cheese&raisins increase |
testosterone:foods like broccoli tyramine:cheese&raisins |
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unilateral/spatial neglect:what it is a problem with |
working memory&shifting attention deficit |
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1.superior longitudinal fasciculus:right hemisphere axon path b/w posterior parietal&prefrontal cortex amplify signal/activity(not in repeat action potential form)from V1 for consciousness&working memory. |
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treat unilateral neglect |
touching increases attention(unless they have sensory loss). so does crossing arms&telling them to focus |
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mind wander networks |
1.Default: |
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Phi Phenomenon |
brain changes what occurred so it makes sense. |
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masking:2 types |
mask:long stimuli designed to reduce visibility/interrupt the recurrent interaction of a stimuli |
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masking:word example |
dont register a word if a jumbled screen(mask) is flashed but can register it if screen is blank |
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feedforward sweep isn't changed by mask:activity response interval latancy link w stimuli in |
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hypothalamic pituitary adrenal axis |
*HPA axis:1.sensory info about percieved threat hit amygdala |
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Wernicke-korsakoff syndrome:cause,result&symptoms |
*from thiamine (vitamin B1)deficiency&alcohol:brain cant metabolize glucose&neuron lost/shrink.damage mammillary body&dorsomedial thalamus.Symptom of prefrontal cortex damage:apathy, confused,forgetful&confabulate.most anterograde w some retrograde amnesia.overlaps w hippocampal damage w episodic memory damage not implicit |
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confabulate |
symptom of korsakoff syndrome:ppl aren't aware that their memory is impaired&fill memory gap w guess(often past event) |
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amnesia:what is damaged,famous example |
damage hippocampus&surrounding medial temporal lobe.cant imagine future&past. |
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alzhiemers:who,onset&symptoms |
1/2 ppl 85+.1/2 w genetic cause(esp. w early onset:5%are ~74).often seen in downsyndrome adult:confused,fatigue,depressed,restless, hallucinate,delusion&appetite loss.gradual progressive memory loss(bad explicit.ok implicit). |
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tau phosphorylation:intracellular neuron support system join&hold axons microtubes in place |
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*plaque *tangle *net effect *atrophy |
1.plaque:clump from degenerate neuron from beta net effect:beta activity cause damaged dendric spines&less synaptic input&plasticity *atrophy:means to waste away |
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attack in dendrite magnify damage. |
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2 types drugs for alzhiemers:effective |
not very effective.most block enzyme that degrade ach stimulates its receptor/prolong release for more arousal.2.curcumin(tumeric:indian spice)may help:inhibit beta deposit&phosphate attached to tau |
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*healthy prefrontal cortex *working memory |
respond fast to recent event b/c working memory (stores event representation).galvanic skin response(change conductance/sweat)b4 unethical/bad decision:switch to good(dont use logic for moral b/c of empathy). |
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2 cells in the prefrontal cortex& their role in response |
1.ventrolmedial cell responds based on expected rewards from past experiences 2.orbitofrontal cell responds based on how reward compares to the alternative choice. plays a role in self control ex.$2 is good/bad depending on if the other choice is $1 or $5 |
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amnesia:effect on memory |
there are many independent kinds of memory that depend on different brain areas(arent lost =ly). |
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1.antrograde:can't form new long term memories |
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1.mirror drawing task:must write in mirror. it is hard at first but they have implicit procedural memory so long as their basal ganglia is ok. they improve over trials without conscious awareness |
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A.B Baddley&G.J.Hitch |
studied working memory:we store info while we work w it.cells store extra Ca which increase readiness to respond to new signals |
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original belief regarding consolidation |
*thought brain consolidated info after it got the necessary proteins |
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what is aplysia&why is its neurons are easily studied |
*1 celled sluggish marine invertebrate. |
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3 hypotheses on the function of hippocampus *what memory is impaired the most by damage |
1.Larry squire:hippocampus involved in episodic memory **impair new learning the most |
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2 animals that'd have more hippocampus activity according to the 2nd hypothesis |
spatial learning activates more of the right posterior area in taxi drivers&birds that depend on locating things |
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2 mazes for rats that test spatial abilities&rational learning *2 reasons a rat wouldn't be able to do it |
1.radial maze:central point w 8 arms.Rat recall which arms had food/shocks by the ones explored,room cues&ones that never do(rough floor) *can't do after hippocampus damage/rearranging |
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contextual memory |
from configural learning |
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2 main types of long term memory |
1.explicit/declarative memory:conscious,verbal deliberate recall.categories:episodic(like autobiographical)&semantic |
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2 main brain areas looked at for implicit memory learning if the CS ends before the onset of the UCS in a memory trace condition |
1.cerebellum:balance&body movement control:specialized for brief interval timing.fibers link it to cerebral cortex |
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memory type parkinsons ppl are missing&why |
dont have implicit memory b/c they damaged their basal ganglia |
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2 types of explicit memory:the question they ask |
1.episodic:single personal event memory(autobiographical:time,place,emotions,age&context) involved the hippocampus.asks what happened? |
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semantic dementia |
damage to anterior&inferior temporal lobe regions(usually w age). cause ppl to lose word concept. ex. call a zebra a horse |
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engram:definition |
physical location of pavlovs connection for learning. |
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engram:karl lashley:2 wrong assumptions |
assumed:engram is in cerebral cortex&more is best&all memory kinds are physiologically equal. |
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Richard thompson: with a deactivated ____, a rabbit can't learn. *with a deactivated____, a rabbit can't express what it has learned |
LIP needed to learn red nucleus is needed to express what they have learned |
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nonassociative learning:implicit |
Habituate:response to the same repeated,harmless stimulus gets weaker |
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procedural implicit memory |
form a habit/motor skill. asks the question 'how to' |
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associative implicit learning:the 2 types&who discovered them:2 similarities b/w their beliefs |
*thought you couldn't study consciousness. wanted to control behavior |
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pavlov's classical conditioning:3 steps |
1.we're born w link b/w unconditioned response(salivate)&unconditioned stimuli(food). |
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thought controlling behaviour was needed for eutopian society.learn/response probability increases if reinforced&decreases if punished.d |
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erik kandel
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studied neural path:touch receptor to other cells to motor cell to direct response.
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Kandel's aplysia study:the results of habituation&control |
1.control:average motor&sensory neuron nts release&avr withdraw |
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Kandel's study:reaction he was studying *stimuli he used:what are the 2&what was used in each of 3 conditions
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studied aplysia's gill withdraw reaction in 3 conditions *used water jet on siphon as tactile stimuli *other stimuli was shocking tail 1.control:1 jet 2.sensitization:1 shock followed by jet 3.habituation:repeat jet |
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Kandel's study:sensitization condition result |
*more sensory& motor neuron nts release.*interneuron released serotonine(5HT block membrane k channel so it takes longer to depolarize w later action potentials)to presynaptic sensory terminal.*k leaves sensory cell slow&it releases nts longer.repeat=sensory cell synthesize new protein for longterm sensitization(molecular even behaviour plasticity) |
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3 main differences b/w short&long term memory |
1.LTM has an unlimited potential capacity/storage space.STM is limited to 5-9 items |
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memory model: |
1.sensory memory store sensory input(hear,see,touch)for 1-2sec. |
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consolidate |
low-moderate cortisol activate amygdala&hippocampus to consolidate&store new experience.high level(from stress)impairs memory |
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reverberate neuronal activity circuit over time:if event reactivates memory,connections become temporarily labile&unconsolidated.emotion influences&changes or extinguishes memory(rely more on cerebellum |
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Hebbian synapse |
donald hebb:simplified definition of LTP:action potential:axon A(slight stimulate B)&axon C(strong stimulate B)fire for paired activity:combined effect on axon B increase effect/ability to stimulate B in future.when neuron axon A repeated fires to axon B,growth process/metabolic change occurs in 1/both cells to increase A axons ability to excite B. classic condition:CS:A. UCS:B |
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donald hebb:opinion on learning |
learning depend on change at synapses from work w aplysia&rat hippocampus.no 1 mechanism(chemical process)accounts for all b/c brain cant react fast enough to learn immediately. |
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biochemical mechanisms of long term responses |
its hard to isolate chemical change at 1 of many tiny neuron synapse(per neuron) so its hard to determine LTD<P. *balance brains energy:if 1 synapse strengthens.1 weakens so brain uses same energy. |
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LTD& LTP |
1.LTD:depression:long term response at synapses decreases if axons are less active than others
2.LTP:reflects increased activity by presynaptic neuron & increased responsiveness by postsynaptic neuron:found most readily in hippocampus |
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hippocampus *where input enters *where output leaves |
input enters hippocampus through ordinal cortex(under the amygdala) *it exits through the fornix |
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2 changes that long term potention depend on |
*change at GABA synapses *change at glutamate synapses |
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5 steps in long term potention:chemical names only
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1.axon repeatedly release glutamate 2.AMPA receptor open Na channel 3.magnesium ions leave 4.NMDA receptor open Ca&Na channel 5.chemicals:CaMKII,CREB,BDNF |
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4 possible postsynaptic cell outcomes in LTP |
a)dendrite make more&rearrange old AMPA receptors |
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glutamate:what it is&its role in LTP |
axon repeatedly release it(most abundant transmitter):it attaches to an ionotropic glutamate type receptor(AMPA or NMDA:abundant in brain)to open channels&let ions enter postsynaptic cell |
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AMPA receptors role in LTP |
1.typical receptor respond to drug AMPA:opens channel to Na enter. |
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depend on membranes polarization: |
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NMDA receptor:drugs blocking its synapses 4 effects of mice mutation:so theres more NMDA receptors *drug it responds to |
1.better memory. 2.learn fear fast&can't unlearn it 3.learn hard mazes faster but simple mazes slow 4.have chronic pain *drugs stop LTP from establishing but not its maintenance *it responds to NMDA drug |
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2 chemicals for LTP formation/maintenance
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1.CaMKII sets reaction series in motion to release CREB protien |
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chemical that magnifies the effect of CaMK11&CREB for LTP |
BDNF:brain derived neuropotropic factor released by persist synapses activity cause action potential:start in axon&back propogate into dendrite):for synaptic plasticity,learning&neuron proliferation,growth,survival&connections in hippocampus.damage cause small hippocampus,impaired learning&few new neurons |
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3 properties that make LTP attractive for cellular learning basis:names only |
1.specificity |
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Specificity:LTP property |
only synapses on highly active cell are strengthened/potentiated(more responsive to new input of that type).more chemical change at synapses mark it for later identification by chemical circulating through cell so genes know to strengthen it |
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Associativity learning:LTP property |
response to axon 2(weak)pair w rapid stimulation in axon 1 input cause strong dendrite depolarization&enhanced both axons response later b/w presynaptic axon&postsynaptic dendrite |
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Cooperativity:LTP property:2+axons |
repeated simultaneous stimulation *by 2+ axons (presynaptic&postsynaptic cell activity)side by side on dendrite makes LTP w a big EPSP spatial sum:changes synapse effectiveness. |
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2 Drugs that effect LTP& learning |
*inhibit LTP production weaken memory help memory by enhance LTP |
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how people remember best:2 times activity increases in brain areas |
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Sherrington&Cajal study on LTP |
extensive post synaptic cell stimulation cause retrograde transmitter NO(nitric oxide)released to travel back.it modifies presynaptic cell to decrease action potential threshold&increase nts release(from more/expanded sites on axon) |