Psych 261 Final Exam

Front 1

major depression
*polarity
*episode statistics:time length,prevalence,onset,cause

Back 1

unipolar depression characterized by extreme low lasting a few weeks-few months if untreated
-10% of people get at least 1 episode(most common in women over 14)
-1st episodes triggered by a stressful episode(only slightly increases risk without genes)&makes future episodes more likely

Front 2

6 common causes for major depression

Back 2

1.interacting genes
2.viral infections
3.hormones
4.sleep problems
5.strong right prefrontal activity
6.less BDNF

Front 3

genes that increase depression risk for each syndrome

Back 3

1.early onset:b4 30yo:have relative w anxiety,depression,adhd,alcohol,bulimia,migraines,ocd,weed addiction&irritable bowel syndrome)
2.late onset:45+have relative w circulatory issue

Front 4

borbona disease

Back 4

viral infection found in 1/3 of ppl with depression&schizophrenia.infection in farm animals cause alternating frantic&inactive states

Front 5

8 hormones involved in depression(5 categories)

*4 hormones in women

*1 in men

*2 in both

Back 5

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
M:3.less testosterone
both:4.serotonin(decrease w diet dont cause depression)but 2 short forms increase risk.

5.catecholamines:dopamine&norepinephrine

Front 6

hemispheric dominance in depressed people
*what it causes
*statement on what depression is based on it

Back 6

have more stable activity in prefrontal right cortex regardless of symptoms.causes change in synapses to nucleus accumbens which make it unresponsive to reward.
*happiness absence increase sadness(report avr #-ve moment)

Front 7

insomnia&depression
*stat
*REM difference
*hormone change
*solution

Back 7

1/2 of teens w insomnia get depressed in 6yrs.
*enter rem in 45min earlier w more eye movement.
*sleep deprivation cause astrocytes to release adenosine(antidepressent effect).
*solution to alter sleep schedule

Front 8

typical antidepressants work
*what they release
*prescription process
*2 issues

Back 8

vary in targeted nts but all increase BDNF&seretonin nts release
*prescribe new 1 every 6 weeks to find 1 that works.all types&ones in type are =ly effective.
issues:1.big antidepressent theoretical difficulty:effect nts in synapses within min-hrs but take 2 weeks for mood elevation.
2.can cause mania

Front 9

atypical antidepressant

*catechomines in depression

Back 9

dont release seretonin:inhibit catechomine(dopamine&norepinephrine) reuptake.

Front 10

4 typical antidepressent categories

Back 10

1.tricylics
2.SNRI
3.SSRI:
4.MAOI:

Front 11

tricylics:6 things they block&treat.side effects

Back 11

treat depression:block transporter protein that reabsorb serotonin&catecholamines into presynaptic neuron after release to prolong nts presence in synaptic cleft&stimulate postsynaptic cell.
*block histamine(organic nitrogen compound act as nts:fatigue),ach(dry mouth,trouble peeing)receptor&Na(<3 issue) channel

Front 12

2 reuptake inhibiters for depression

Back 12

1.SNRI:block serotonin &norepinephrine reuptake
2.ssri:block serotonin reuptake.like tricyclics w less side effect

Front 13

MAO inhibiter for depression
*what can't you eat&why
*what it blocks
MAO definition

Back 13

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.

Front 14

2 depression treatments that act on glutamate receptors

Back 14

1.ketamine antagonize NMDA receptors&increase new synapse formation for rapid antidepressant effect:cause hallucination&delusion
2.L-acetylcarnitine:epigenetic change on glutamate receptors.

Front 15

st. johns wort
*2 pros&2 cons
*how it works

Back 15

cons:herb isnt regulated&purity varies by bottle.
pros:inexpensive&available wout prescription.
*increase enzyme(that break down plant toxin in liver&meds)effectiveness

Front 16

placebos effectiveness to treat depression&their limit

*relation to how brain stimulation treatment works

Back 16

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

Front 17

brain stimulation for depression
*4 types(2 are described)

*retrograde amnesia

Back 17

1.ECT&repetitive transcranial magnetic stimulate:new neuron proliferation&alter 120+gene expression in hippocampus&frontal cortex.cause retrograde amnesia
2.deep brain stimulate:implant battery power device in brain to stimulate areas activated by antidepressants.in experiment phase.possible refinement:optogenetic stimulation control individual connections not all axons from 1 area to other

Front 18

bipolar disorder:prevalence, gender/age vulnerability
*other name

Back 18

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

Front 19

the 3 episodes/2 bipolar disorder types

Back 19

depression is paired w 1 other episode type
bipolar 1:full manic episode:restless activity,excited,laughter,excess self confidence, rambling speech&inhibitions lost.are danger to self&others
bipolar II disorder:hypomanic episodes(mild manic:anxiety&agitation)

Front 20

hormones involved in bipolar disorder:2 of them

Back 20

*people alternate b/w 2 poles:mania:brain increase &A receptor(which increases glutamate&glucose)
depression:brain decrease glucose

Front 21

lithium salt
*what it treats
*who/how it was discovered
*what it does
*problem

Back 21

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

Front 22

anticonvulsant
*2 types
*when they work best
*what they treat

Back 22

valproate(depakote)&carbamazepine less effective but treat bipolar disorder.pair w antidepressant

Front 23

how bipolar treatments help

Back 23

1. decrease AMPA receptor # to decrease glutamate.
2.block brain chemecial arachidonic acid synthesis(form w brain inflammation in all cell membranes)

Front 24

why seafood helps treat bipolar disorder

Back 24

counter acts arachidonic acid synthesis b/c it is an omega 3 polyunsaturated fatty acid

Front 25

seasonal affective disorder:what is it,where it is seen&treatment(how it works)

Back 25

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

Front 26

sleep pattern of depressed/bipolar vs someone with SAD:possible cause

Back 26

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

Front 27

brain stem:what it does&1 structure it contains(&its function)

Back 27

processes salient(a strong/noticeable) event.
*reticular formation:involved in alertness&consciousness

Front 28

function of the corpus callosum&what it is

Back 28

bundle of fibers responsible for communication b/w hemispheres

Front 29

processing emotion:what it consists of
*relevance of facial paresis(2 types)

Back 29

2 independent processes join for a double process.evidence in facial paresis
1.Emotional paresis:can voluntarily move face not naturally.damage PFC,thalamus &white frontal lobe matter.
2.Volitional paresis:naturally move face not voluntary.damage motor cortex&subcortical connection.

Front 30

autonomic nervous system:2 branches

Back 30

involved in different combo for all situations.
1.sympathetic autonomic NS:neural arousal causes emotion(joy,mad,fear) w autonomic physical response.
2.parasympathetic autonomic NS:more digestion&processes save energy&prepare for later event.

Front 31

sympathetic autonomic nervous system:role in fear
*gut feeling

Back 31

hypothalamus causes fear(<3&blood rate increase)which leads to panic attack if extreme arousal.ppl that detect their autonomic response consciously identify danger.

Front 32

pure autonomic failure
*cause
*symptom/response

Back 32

symptom/response:feel less intense/no emotion but claim to empathize.
*organ activity isnt controlled by output automatic nervous system

Front 33

theories of emotion:according to 3 components of emotion
*ppl who created them (5ppl)

Back 33

after you perceive a stimulus:
1.james lange:skeletal action influences feeling
2.walter cannon&bard:action&feeling are simultaneous
3.schachter&singer:feeling causes you to assess situation(cognition)&then act

Front 34

james lange opinion on emotion
*example
*smiling evidence:lab study&real life example

Back 34

emotion are embodied&used to label experience.ex. you run b/c you're afraid
smiling example:1. pencil b/w teeth causes joy
2.people w botox can't frown so they take longer to interpret unhappy sentences

Front 35

walter cannon discovery related to autonomic nervous system

Back 35

1st to know sympathetic autonomic nervous system prepares you for fight/flight

Front 36

emotion components:issue w theory

Back 36

1.action impulse:physical response.
2.cognition:appraise/assess situation
3.feeling:subjective/general arousal.
issue:hunger&thirst arent emotions but fit description

Front 37

emotions as motivations:explanation&issues

Back 37

internal processes modify response to an external stimuli class.issue:joy,fear,sad aren't motivations

Front 38

is emotion localized in brain
can you identify specific emotions

Back 38

emotion is all over brain.can identify whether an emotion is -ve or+ve but not specific emotions

Front 39

limbic System:location&what its critical for

Back 39

forebrain area around thalamus is critical for emotions

Front 40

insular cortex:location,what it interprets&damage

Back 40

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

Front 41

evidence against james lange
*mobius syndrome
*paralyzed

*method acting

Back 41

*can feel emotions to same degree but can't express them:

1.Mobius Syndrome:cant smile/move facial muscles.
2.paralyzed:have cranial nerve damage

*method acting:make self feel emotion to show natural reaction

Front 42

amygdala:3 roles(when it works best)

Back 42

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).
2.direct brain area to recall,attend&respond to event.
3.more active amygdala in corticomedial area is linked to escape&attack behavior

Front 43

amygdala w high response linked to 2 things

Back 43

1.agreeable w police(perceive&try to protect from protect from danger)
2.jobs in&high combat stress in military.

Front 44

damage amygdala:3 general results
2 disorders/syndroms
*1 individual

Back 44

1.cant rate,draw®ister emotional stimuli(include surprise)b/c dont attend eyes.*SM find uncomfortable stuff to be comfortable
2.cant anticipate unpleasant outcome.
3.activity&fear varies:a)Kluver Bucy syndrome:tame&placid. b)Umbach-Weithe Disease(from skin lesions)are fearless.

Front 45

escape behavior:what amygdala axon does
*2 fear reactions it causes&their definition

Back 45

axon send input from pain,vision,hearing down 1 of 2 paths to cause
1.startle reflex:fast responst to unexpected stimuli.ex.loud noise is prebuilt fear
2.conditioned fear:long term generalized arousal in various situations from a traumatic experience

Front 46

pathway for conditioned fear:3 parts

Back 46

circuitry
1.amygdala axon
2.bed nucleus stria terminals(join central&basolateral nuclei to amygdala axon
3.hypothalamus

Front 47

startle reflex pathway
*6 steps(7 brain parts)
*damage result
*conditioning
*time it takes

Back 47

take 0.2seconds: 1.amygdala axon
2.brain stem
3.cochlear nucleus in medulla(midbrain)&prefrontal cortex(fight/flight)
5.pons
6.tense (neck) muscle.
*damage:interfere (stop if pon damage)w it. reverse startle to -ve event w +ve conditioning.

Front 48

attack behavior
*what is it
*2 things that increase risk
*ASPD is caused by combo of 3 things

Back 48

anger&aggression:increase w
1.# of previous attacks&if standing.
2.triple imbalance hypothesis
*ASPD is combination of MAO,genes&experience

Front 49

triple Imbalance Hypothesis for attack behavior:3 chemicals it depends on

Back 49

#1.low cortisol:low fear.
#2.high testosterone:more emotion link area response&less cerebral cortex able to consciously identify it(gradient to anger).#3.low serotonin:cant inhibit impulse.cause depression,violent suicide&drug crave.

Front 50

hydroxyindoleacetic acid:what it is&its role in aggression
*turnover rate

Back 50

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.

Front 51

tryptophan influence on men
*isolation
*diet

Back 51

isolation cause inactive tryptophan(amino acid in protein synthesizes serotonin.is controlled by genes)hydroxylase which lowers seretonin:*tryptophan cross blood brain barrier w active transport channel shared w phenylalanine.big acid diet intake lowers serotonin synthesis.

Front 52

2D-4D ratio

Back 52

ratio b/w index &ring finger shows testostrone levels from utero (used to stop miscarriages)

Front 53

prefrontal cortex role in attention&memory
*where it gets input
*parts&what happens if they are damaged

Back 53

*get input from dorsomedial thalamus.
*middle frontal gyrus direct attention(active to suppress distraction&speed up trial at start).lose memory if its old,damaged&inactive
*anterior:source amnesia(lose specific episode memories) if its damaged w cingulate cortex

Front 54

damaged prefrontal cortex:4 impact on decision making/ emotion
*2 damaged types

Back 54

lesion&kid:1.make impulsive/irrational choice wout consequence thought for fast reward
2.no emotion except anger burst(antonia damasio).
3.guilt deficit:dont share $.
4.take more time to consciously register visual stimuli.

Front 55

4 moral dilemmas:how ppl w damaged amygdala,prefrontal cortex &cingulate gyrus respond

Back 55

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)

Front 56

ioga gamble experiment:who studied it

*results

Back 56

*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

Front 57

frontal/temporal lobe/cortices activity
*importance
*difference

Back 57

1.important for wide emotion range.
2.Difference their amount in hemispheres is linked w personality&broken into 2 behavioural systems

Front 58

behavioral activation system
*hemisphere w more frontal/temporal activity
*response
*arousal
*personality

Back 58

BAS:left hemisphere has low-moderate arousal.approach(fight).high prefrontal activity:happy,outgoing,fun love

Front 59

behavioral inhibition system
*hemisphere w more frontal/temporal activity
*response
*arousal
*personality
*damage

Back 59

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

Front 60

anxiety:amygdala(not always abnormal)&hypothalamus.
Panic Disorder prevelance
*5 causes

Back 60

in teens&Women
1.abnormal amygdala(usually)&hypothalamus
2.genetic
3.high CCK (cholecystokinin)level&transmitter orexin.
4.less nts active GABAa

Front 61

chl in panic disorder
*alcohol role

Back 61

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.

Front 62

treat for panic disorder

Back 62

no drug target.block learned fear/avoid behaviour:
1.Benzodiasepine
2.propranolol approach

Front 63

Benzodiasepine for anxiety:how it works, side effects, result

Back 63

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.

Front 64

propranolol for anxiety:who it helps,what it does

Back 64

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

Front 65

David Chalmers

Back 65

came up w 2 problems
1.hard problem:scientifically hard but philosophically easy:why does consciousness exist
2.easy problem:what is consciousness(the difference b/w sleep&awake)

Front 66

Mind-Brain Relationship
*why it was raised&example
*what it means
*2 belief categories&who believed the less modern one

Back 66

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

Front 67

3 categories of monoism

Back 67

1.materialism:all that exists is material/physical&psychalogical experiments are explained w physical terms.
2.Eliminative:extreme materialist view believe mental events dont occur
3. Identity Position:Mental&brain processes are same thing described differently.Ex:list every color point on Mona Lisa painting.mind is brain activity.brain activity doesnt cause consciousness more than consciousness does brain activity.

Front 68

consciousness according to biology:frequency,brain areas involved, waves

Back 68

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

Front 69

consciousness according to psychology
*issue

Back 69

cooperative ppl report a stimulus that theyre aware of
*issue if ppl can’t speak(baby&ppl w Brocha’s Aphasia).ex.vegetative state ppl show right brain area activity on fmri if asked to imagine task(unsure if they're conscious).

Front 70

Binocular Rivalry
*example w gyrus response to faces&places
*time involved

Back 70

brain switches focus b/w different images sent by each eye individually.occurs roughly every 2 seconds on avr
ex.shift perception shifts fMRI brain activity b/w FFA(fusiform gyrus when you respond to a face)&PPA(parahypocampal gyrus when you respond to a place)

Front 71

Inattentional/change blindness

Back 71

something complex in scene changes slowly/when you blink&you dont notice&are unaware of obj in full view

Front 72

bottom up attention
top down attention(include main brain part)
which is a video gamer best at

Back 72

Bottom-up attention:Reaction to stimulus
Top-down attention:Intentionally focusing on stimulus(use prefrontal cortex).
*video gamers are good at top-down attention

Front 73

what type of phenomenon is consciousness&why

Back 73

a yes-no phenomenon b/c you can't be unaware&aware at the same time

Front 74

what broccoli increases

what cheese&raisins increase

Back 74

testosterone:foods like broccoli

tyramine:cheese&raisins

Front 75

unilateral/spatial neglect:what it is a problem with
*is it a right-left dimension
*2 studies

Back 75

working memory&shifting attention deficit
*no right-left dimension b/c damage to left dont cause opposite.although mostly distracted from/ ignore stuff on left,can also ignore obj on right
ex:sound:cant tell which is 1st unless 2 are prolonged.
point to right of obj instead of center:ppl usually point 3%to left

Front 76

unilateral neglect:3 areas w brain damage

Back 76

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.
2.inferior parietal cortex(join memory pieces):ignore left side of body.
3.superior temporal cortex:ignore obj

Front 77

treat unilateral neglect

Back 77

touching increases attention(unless they have sensory loss). so does crossing arms&telling them to focus

Front 78

mind wander networks
3 in 1st
2 in 2nd

Back 78

1.Default:
B:ventral anterior cingulate cortex.
C:precuneus.
D:bilateral temporoparietal junction
2.Executive:
A:dorsal anterior cingulate cortex.
E:bilateral dorsal lateral prefrontal cortex(DLPFC)

Front 79

Phi Phenomenon
*examples&what it is

Back 79

brain changes what occurred so it makes sense.
ex:dot jumps across screen:ppl think it moved.
ex:word like dent/tent is heard based on sentence meaning(hear dent for car&tent for camp)

Front 80

masking:2 types
*mask definition

Back 80

mask:long stimuli designed to reduce visibility/interrupt the recurrent interaction of a stimuli
1.forwards:mask is flashed after brief stimuli.
2.backwards:stimuli is shown after a mask

Front 81

masking:word example
*color example

Back 81

dont register a word if a jumbled screen(mask) is flashed but can register it if screen is blank
2.red stimuli(for 40ms) followed by blue will reduce reds visibility

Front 82

mismatch recurrent&feedfoward info effect for masking
*3 areas linked w latency(what latency)

Back 82

feedforward sweep isn't changed by mask:activity response interval latancy link w stimuli in
1.FEF(frontal eye field)
2.inferior temporal cortex(activated by red at 100ms:send feedback to low area)
3.V1(activated by mask:feedback dont match low-level activity)

Front 83

hypothalamic pituitary adrenal axis
*4 steps(or 5)
*mood/anxiety disorder effect

Back 83

*HPA axis:1.sensory info about percieved threat hit amygdala
2.hypothalamus release CRH&anterior pituitary release ACTM.3.adrenal gland release cortisol to prep body for fight/flight.
4.hippocampus receptor sites send feedback to hypothalamus to inhibit excess cortisol(unless you have mood/anxiety disorder

Front 84

Wernicke-korsakoff syndrome:cause,result&symptoms

Back 84

*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

Front 85

confabulate

Back 85

symptom of korsakoff syndrome:ppl aren't aware that their memory is impaired&fill memory gap w guess(often past event)

Front 86

amnesia:what is damaged,famous example

Back 86

damage hippocampus&surrounding medial temporal lobe.cant imagine future&past.
H.M:1953 surgery lowered seizures(~2/yr):had retrograde b4 surgery&anterograde amnesia after&emotional placidity.had semantic memory:didnt effect IQ, personality&language ability

Front 87

alzhiemers:who,onset&symptoms

Back 87

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).

Front 88

name&description of 2 proteins involved in alzhiemers

Back 88

tau phosphorylation:intracellular neuron support system join&hold axons microtubes in place
2.amyloid beta enzyme

Front 89

alzhiemers:relevant terms

*plaque

*tangle

*net effect

*atrophy

Back 89

1.plaque:clump from degenerate neuron from beta
2.tangles:structures from degenerate structure in neuronal body from tau

net effect:beta activity cause damaged dendric spines&less synaptic input&plasticity

*atrophy:means to waste away

Front 90

2 protein&their effect in alzhiemers

Back 90

attack in dendrite magnify damage.
#1.tau malfunctions&increase causing issue.
#2.increases beta activity:accumulate in&around cell(net effect spread atrophy cerebral cortex, hippocampus&other area).
#3.cause plaque&phosphate molecule to join& disconnect tau(cant bind to target in axons).
#4.separate/collapse microtube cause tangles&neuron death.

Front 91

2 types drugs for alzhiemers:effective

Back 91

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

Front 92

prefrontal cortex role in response
*skin response

*healthy prefrontal cortex

*working memory

Back 92

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).

Front 93

2 cells in the prefrontal cortex& their role in response

Back 93

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

Front 94

amnesia:effect on memory

Back 94

there are many independent kinds of memory that depend on different brain areas(arent lost =ly).
***bad anterograde(for declarative memory)&some retrograde(for episodic info) amnesia.
***normal procedural&working/STM memory

Front 95

3 types of amnesia

Back 95

1.antrograde:can't form new long term memories
2.retrograde:can't recall previously learned information
3.acute transient global amnesia:temporary hippocampus dysfunction cause short term amnesia

Front 96

prefrontal damage
*measure for procedural memory
*measure for declarative memory

Back 96

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
2.delayed sample to sample task:must find the match/nonmatch for an object after a short delay.they can do it b/c they have STM

Front 97

A.B Baddley&G.J.Hitch

Back 97

studied working memory:we store info while we work w it.cells store extra Ca which increase readiness to respond to new signals

Front 98

original belief regarding consolidation
*2 issues with it

Back 98

*thought brain consolidated info after it got the necessary proteins
1.emotionally charged info is easier to put in LTM than unexciting info:time varies for consolidation
2.consolodated facts don't last forever

Front 99

what is aplysia&why is its neurons are easily studied

Back 99

*1 celled sluggish marine invertebrate.
neurons are studied b/c they are big&identical in all aplysia. They're also isnt many of them

Front 100

3 hypotheses on the function of hippocampus
*1 name &hypothesis he's part of

*what memory is impaired the most by damage

Back 100

1.Larry squire:hippocampus involved in episodic memory
2.spatial memory
3.contextual memory

**impair new learning the most

Front 101

2 animals that'd have more hippocampus activity according to the 2nd hypothesis
*what section is bigger

Back 101

spatial learning activates more of the right posterior area in taxi drivers&birds that depend on locating things

Front 102

2 mazes for rats that test spatial abilities&rational learning

*2 reasons a rat wouldn't be able to do it

Back 102

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)
2.morris water maze:rat moves from 1 of 4 platforms to escape platform under murky water.

*can't do after hippocampus damage/rearranging

Front 103

contextual memory
*learning type
*hypothesis type
*definition

Back 103

from configural learning
*recall detail best in same/binded external(location)&internal(arousal,drunk)context
*from 3rd hippocampus hypothesis

Front 104

2 main types of long term memory
*5 subcategories

Back 104

1.explicit/declarative memory:conscious,verbal deliberate recall.categories:episodic(like autobiographical)&semantic
2.implicit memory:unaware/unconscious.experience influence on behavior(cant describe/recognize it).categories:procedural&non associative&associative learning

Front 105

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

Back 105

1.cerebellum:balance&body movement control:specialized for brief interval timing.fibers link it to cerebral cortex
2.basal ganglia:for gradual learning about reward value&various acts:slow by avr reward.

Front 106

memory type parkinsons ppl are missing&why

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dont have implicit memory b/c they damaged their basal ganglia

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2 types of explicit memory:the question they ask
*definition
*brain parts involved

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1.episodic:single personal event memory(autobiographical:time,place,emotions,age&context) involved the hippocampus.asks what happened?
2.semantic memory:anterior&inferior temporal lobe region store it as hub to communicate w other areas&join concepts.factual memory for repeated info:ex. elvis' last name. asks what it is?

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semantic dementia

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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
*2 ppl:what they studied

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physical location of pavlovs connection for learning.
1.Karl Lashley:studied rat cerebral cortex by making lesions
2.Richard Thompson:study rabbit cerebellum by cooling

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engram:karl lashley:2 wrong assumptions
*2 nervous system principles
*discovery

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assumed:engram is in cerebral cortex&more is best&all memory kinds are physiologically equal.
1.mass action:cortex units work as a whole
2.equipotentiality:all parts contribute =ly for complex function behaviours(like learning)&substitute for each other
*size of lesion matter more than area

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Richard Thompson engram:3 brain parts&their function
*CS,UCS,CR&UCR role

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*LIP:need to learn CS(tone)&UCS(air puffed into eye)
*nerve VI:abducen:CR&UCR control nictitate membrane movement.
*red nucleus:midbrain motor area get input from cerebellum.needed to show learning

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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

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LIP needed to learn

red nucleus is needed to express what they have learned

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nonassociative learning:implicit
*2 parts

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Habituate:response to the same repeated,harmless stimulus gets weaker
Sensitization:learning type:1 intense stimuli experience heightens future mild stimuli response

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procedural implicit memory
*question asked

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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
*1 difference in their theories

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*thought you couldn't study consciousness. wanted to control behavior
1.classical conditioning:pavlov
2.operant(instrumental)conditioning:skinner
*in operant conditioning, peoples response/behavior determines the outcome

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pavlov's classical conditioning:3 steps

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1.we're born w link b/w unconditioned response(salivate)&unconditioned stimuli(food).
2.conditioned stimuli(apparatus noise:doesn't elicit response on its own)paired w unconditioned stimuli changes response to the conditioned stimuli.
3.conditioned&unconditioned response link in brain but reactions can differ

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operant instrumental conditioning:skinner
*what he thought it'd lead to
*explanation

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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
*4 neural path steps
*what he was interested in studying/hypothesis

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studied neural path:touch receptor to other cells to motor cell to direct response.
*thought behavior changes w experience:trace to change is at identified synapse b/w sensory&motor neuron not from muscle fatigue

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Kandel's aplysia study:the results of habituation&control

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1.control:average motor&sensory neuron nts release&avr withdraw
2.habituate:less motor&sensory neuron nts release.weak gill 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

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*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

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1.LTM has an unlimited potential capacity/storage space.STM is limited to 5-9 items
2.LTM requires no memory strategy&STM requires rehearsal,attending&repetition. 3.LTM is permanent&info is retrieved w hints/cue. STM require memory strategies or you forget in 15-18 seconds

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memory model:
*2 ppl
*4 parts

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1.sensory memory store sensory input(hear,see,touch)for 1-2sec.
2.if attended,info go to STM(Working memory)&held through memory strategies
3.memory is consolidated&changed for LTM/extinguished
4.memory stored in LTM for later retrieval

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consolidate
*cortisol
*brain activity
*explanation

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low-moderate cortisol activate amygdala&hippocampus to consolidate&store new experience.high level(from stress)impairs memory

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reconsolidate:brain parts,what occurs

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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
*who
*what
*axon roles
action potentials
*classical conditioning

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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

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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
*how easy are they to determine
*what they do

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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
*hippocampus relevance

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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

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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

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*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

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a)dendrite make more&rearrange old AMPA receptors
b)dendrite make more branches&spines for more synapses w same axon
c)phosphate group join w&increase AMPA receptor responsiveness
d)neuron make more NMDA receptor

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glutamate:what it is&its role in LTP

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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
*what it opens&responds to
*result if LTP is successful
*magnesium ions role

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1.typical receptor respond to drug AMPA:opens channel to Na enter.
2.Na depolarizes (less -ve charge)dendrite membrane so +ve magnesium ions leave
3.stimulates nearby NMDA receptors
*if LTP's successful, it stays potentiated:has increase response to glutamate later

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NMDA receptor role in LTP
what it opens&responds to
*role of membrane polarization degree
*result if LTP is successful
*result
*drugs

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depend on membranes polarization:
1.membrane at rest potention:magnesium block ion channels& dont fit if glutamate attach
2.if depolarized, it opens channel&Na&Ca enter.
3.Ca activates CaMKII protein
*w LTP success,post&presynaptic cells are polarized(active)w fast firing rate so NMDA reverts to original form.

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NMDA receptor:drugs blocking its synapses

4 effects of mice mutation:so theres more NMDA receptors

*drug it responds to

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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
2.CREB enter cell nucleus& regulate/alter gene expression(last years:account for LTM)

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chemical that magnifies the effect of CaMK11&CREB for LTP
*what its for,causes,is from&damage result

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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

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1.specificity
2.cooperativity
3.associativity

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Specificity:LTP property
*gene factor

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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

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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
1 axon

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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.
* by 1 axon/synapses:total EPSP dissipate b/w small fire rate b4 postsynaptic dendrite so no LTP.w fast fire rate:big EPSP total summed across fires give LTP

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2 Drugs that effect LTP& learning

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*inhibit LTP production weaken memory help memory by enhance LTP
1.Moderate dose stimulant(caffeine,methylphenidate)enhance learn by increase arousal.
2.Ginkgo Biloba:natural herb:Mass study found it was not useful.

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how people remember best:2 times activity increases in brain areas

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Ppl remember better if engaged rather than series of facts thrown at them.activity increases in many brain areas while you are wait for answer. Activity increases when you hear correct answer, if your guess had been wrong.

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Sherrington&Cajal study on LTP

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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)