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Physiological Psychology > Unit 2 lecture > Flashcards

Unit 2 lecture Flashcards

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1
Q

history

A
  • Know what the message is without having to hear it
  • Caller ID and see it’s your boyfriend
  • Dont listen to the message b/c you know what he wants based on history
  • dese anteriorgrade amnesia
    *
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2
Q

pathway

A
  • result of neuromigration during development
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3
Q

history (science explanation)

A
  • neurosculpting
  • start with undifferentiated neurons and then figure out who you are by wiring specific neurons
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4
Q

neural wiring

A
  • dedicated pathways and history
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5
Q

zygote

A

single cell (sperm+egg)

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6
Q

embryo

A
  • 2 or more cells
  • totipotent
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7
Q

stem cell

A
  • have the potential to differentiate into any cell
  • regenerate
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8
Q

totipotent

A
  • ability of single cell to divide and produce all the differentiated cells that make up an organism
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9
Q

In vitro fertilization (IVF)

A
  • inject fertilized egg into female that is infertile, or whose husband is infertile
  • implant multiple to be sure
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10
Q

how does totipotent cell know what to differentiate into

A
  • chemical gradient in uterus
  • chemical composition of cell in uterus, determines what it will become
  • nearest to bottom- neurons (fetus develops with head down)
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11
Q

migration

A
  • neron has to migrate to target in spine
  • genetics and chemical influences determine migration during development
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12
Q

difference between fetus and embryo

A
  • fetus at 3 months b/c start looking human
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13
Q

how does neuron know where to travel

A
  • growth cone serves as “feelers”
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14
Q

retina neurons

A
  • half of cell cross over at ptic chiasm
  • other half dont
  • example of some neurons following signs and others not
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15
Q

3 stages of differentiation

A
  • figure out what cell is going to be
  • strat to migrate
  • when close to target get permiscuous about where you want to be
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16
Q

Retinal signal

A
  • neural cell in retina senses light
  • nerve reaches optic chiasm
  • cells then travel to cortex
  • *spot on retina correlates with spot on cortex (good connection)
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17
Q

bad connection

A
  • signal on retina goes to wrong part of cortex
  • surrounding cells in retina are correct connection and behaving appropriately- releasing neruotransmitters and neurotrophins
  • surrounding cells in cortex are not happy b/c not in the same location as the right cells
  • neural cell of bad connection goes through apoptosis
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18
Q

neurotrophins

A
  • enhance growth
  • Ex: nerve growth factors
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19
Q

apoptosis

A
  • programmed cell death
  • cell only does it when it knows it doesn’t belong
  • leads to the complicated connections and proper cell arrangement
  • Ex: good for eliminating webbed feet and hands of embryo
  • bag organnelles to prepare for release upon bursting and macrophage degradation
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20
Q

necrosis

A
  • cell injury that results in premature death
  • membrane ruptures and dumps organelles into extracellular fluid before they are “bagged”
  • release of free radicals
  • Inflammation
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21
Q

connect to right side of cortex

A
  • turn on and off at the same time as neighbors
  • release and receive neurotransmitters and nerve growth factors at same time as others
  • If iincorrect, don’t do or get stuff at same time as neighbors, so go through apoptosis
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22
Q

Japanese and “r” and “l”

A
  • during development that can distiguish rs and ls
  • as adults can’t hear or say rs and ls differently
  • examples of apoptosis
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23
Q

Canadians vs. Americans

A
  • Americans have lost ability to hear 3 different sounds, but Canadians can
  • Ex: can’t distiguish between about and a boot
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24
Q

learning language

A
  • many connections before age 5
  • connections decrease after 5 b/c cells that aren’t used kill off
  • loose ability to distinguish
  • Ex: why easier for younger kids to pick up numerous languages
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25
Q

Genie

A
  • when made noises she was beaten
  • when found only spoke 2 english words b/c dad and mom didn’t talk to her (just yelled)
  • shows that we have an INNATE tendency to pick up language
  • IQ was above average, but was still unable to pick up language
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26
Q

critical period

A
  • period at which language cortex kills itself after you haven’t picked up a language
  • Genie was 13, so must be before 13
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27
Q

trying on different hats

A
  • during adolescence try different identities
  • whatever you practice at end of adolecence remains, while other cells associated with other things that don’t fit
  • pick your rut well
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28
Q

frontal cortex

A

identity

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29
Q

cigarette companies

A
  • want to recruit adolescence b/c they will kill off cells that don’t encourage smoking
  • stuck with additcted cells
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30
Q

what happens to a developing neuron that fails to reach its target

A
  • would be outlier and not truning on and off simultaneously with surrounding neurons
  • commit apoptosis- genetic tendency
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31
Q

how does neuron find its target

A

chemicals

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32
Q

why don’t most neurons regenerate

A
  • connections are very numerous and complicated
  • no longer have chemical gradient to follow
  • BBB isolates neurons from chemical and pathogenic insults- no exposure means don’t really need to
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33
Q

why do olfactory neurons regenerate

A
  • they are stem cells (other neurons aren’t)
  • connections are simple
  • they are not isolated by BBB
  • exposed to chemical insults for your benefit and protection
  • olfatory neurons have to test for us
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34
Q

what are 3 epochos characterized by massive apoptosis

A
  1. ) prenatal- before birth
  2. ) paranatal- after birth
  3. ) age 21- find identity then other connections not used die
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35
Q

what happens if inject NGF (nerve growth factor) antagonist into developing brain

A
  • massive widespread brain damage
  • none of the cells think they are connected in the right way
  • in a normal cell, only the nerves that think they are not normally connected kill themselves
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36
Q

turpsichore

A
  • goddess of dance
  • chorea from Huntington’s chorea
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37
Q

Huntington’s chorea

A
  • dominant and lethal
  • lose inhibitory -> everything you do is excitatory
  • always overshoot destination
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38
Q

incest

A
  • bad for genome to have sex with close relation
  • may express lethal genes that could have been avoided by having sex with someone who wasn’t related
  • if both heteroygous, 1/4 chance of having a kid with lethal genes
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39
Q

homozygous for dominant w/ heterozygous for lethal

A
  • no kids express double recessive lethal version
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40
Q

Hapsberg

A
  • kept mating with each other so more and more prominant jaw
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41
Q

mutations

A
  • maladaptive
  • lethal
  • most often recessive
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42
Q

arranged marriage where you meet on wedding night

A
  • more successful
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43
Q

preventing recessive expression

A
  • repeled from people you don’t want to have sex with (close relatives, friends)
  • genes don’t want to have sex with closely related
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44
Q

arranged marriage with childhood acquaintance

A
  • less successful b/c genes don’t like to have sex with closely related
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45
Q

combination of excitatory and inhibitory

A
  • essential for every move you make
  • don’t get to destination as fast, but get there effectively and don’t overshoot (as would if only excitatory)
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46
Q

only have excitatory movements

A
  • consequence of drinking b/c alcohol suppresses inhibitory senses
  • cells don’t repolarize
  • overshoot destination
  • ex: swining door- spring only
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47
Q

door w/o spring and shock absorber

A
  • spring- excitatory
  • shock absorber- inhibitory
  • stimulates motor neurons
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48
Q

how can lethal gene be dominant

A
  • lethal at onset
  • lethal genes passed on to kids
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49
Q

Parkinson’s disease

A
  • dopaminergic cells in substantia nigra fail to release dopamine -> can’t move
  • loss of dopaminergic cells
  • typical onset after 45 years old
  • movement can be initiated by external influences
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50
Q

parkinson’s and movement

A
  • can’t initiate movement on your own- internally
  • externally- initiated actions are possible though
  • Ex: once complete first step, can go up all of them
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51
Q

MPTP

A
  • injection similar to heroin
  • one guy became paralyzed in rigid state- heroin paralysis is sloppy, not rigid
  • targets dopamine reuptake transporters
  • representation of what occurs with parkinson’s
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52
Q

addictive drug

A
  • targets dopamine
  • cocaine, alcohol, heroin, etc
  • Marijuana and LSD NOT addictive
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53
Q

dopamine action

A
  1. ) dopamine release
  2. ) dopamine transporter release
  3. ) dopamine & transporter to soma
  4. ) in soma dopamine removed and recycled (repackaged)
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54
Q

blocking dopamine transferase

A
  • caused by MPTP in synapse
  • affinity of MPTP and dopamine transporter molecule is much greater than transporter affinity for dopamine
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55
Q

MPTP and dopamine transporter

A
  • high affinity
  • blocks up mitochondria
  • cell can’t function w/o mitochondria
  • dopaminergic cell dies
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56
Q

treat parkinson’s

A
  • L-dopa
  • stem cells
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57
Q

L-dopa

A
  • can cross blood brain barrier, unlike straight up dopamine
  • dopamine “bisquick”
  • remaining dopaminergic cells can use to make dopamine effectively w/o having to start from scratch
  • temporary treatment for parkinson’s b/c dopaminergic cells will continue to die
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58
Q

reason for reduced prevealence of Huntington’s

A
  • gene testing lets person know they have the lethal gene and could pass it on
  • most people won’t have kids and take risk
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59
Q

will we all develop parkinson’s

A

yes b/c dopaminergic cells die off over time

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60
Q

negative symptoms of schizophrenia (SZ)

A
  • lacking something normal people have
  • flat affect
  • catatonia
  • waxy flexibility
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61
Q

substantia nigra

A
  • part of midbrain that plays a role in reward, addiction, and movement
  • death of dopaminergic neurons leads to Parkinson’s
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62
Q

dopamine and substantia nigra

A
  • loss of dopaminergic neurons in substantia nigra results in Parkinson’s
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63
Q

schizophrenia

A
  • mental disorder characterized by a breakdown of thought processes and deficit of typical emotions
  • Eugen Bleuler defined as split-mind
  • NOT multiple personality disorder
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64
Q

diagnosing sz

A
  • negative and positive symptoms
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65
Q

positive symptoms sz

A
  • have something extra that normal people don’t have
  • NOT such a good thing
  • psychotic cluster
  • disorganized cluster
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66
Q

affect

A

expression of feeling or emotion

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67
Q

psychotic cluster

A
  • positive symptom sz
  • generally expressed by age 30
  • hallucinations- generally auditory
  • delusions
  • paranoia
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68
Q

auditory hallucination

A
  • think hearing things but not
  • auditory context IS active
69
Q

delusion

A
  • false belief
70
Q

catatonia

A

state of neurogenic motor immobility, and behavioral abnormality manifested by stupor

71
Q

paranoia

A

expectation of conspiracy

72
Q

disorganized cluster

A
  • inability to keep self together
  • invovles abnormal thinking and hygiene
73
Q

causes sz

A
  • genetics
  • prenatal stress- flu, famine, etc
  • dopamine hypothesis
74
Q

monozygotic twins raised apart

A
  • control nature (biology) and manipulate nurture
  • identical twins
  • 75% sz concordance rate
75
Q

dizygotic twins raised together

A
  • manipulate nature (genes) and control nurture
  • faternal twins- different genes
  • sz concordance rate is 25%
76
Q

concordance rate

A
  • have schizophrenic
  • what are the odds relative has sz
77
Q

do you inherit sz

A
  • no, the concordance rate would be 100%, but it’s not
  • you inherit a sensitivity to sz (diathesis)
78
Q

diathesis stress model of sz

A
  • inherit sensitivity to sz
  • increased chance if exposed to stress
79
Q

stress during prenatal development

A
  • second trimester during flu season
  • mother stress, causes fetus to experience stress
  • stress increases chance of sz
80
Q

likelihood of sz if born in flu season

A
  • March, April, May
  • higher likelihood than childrne born in other months b/c of maternal stress during flu season
81
Q

prevelance of sz

A
  • increased for those born 3 months following flu season
  • northern hemisphere- march, april, may
  • southern hemisphere- sept, oct, nov
82
Q

Starvation Winter

A
  • massive famine throughout Holland
  • prevelance of sz increased following famine- when pregos had babies
  • consequences of being in womb during starvation winter (stress)
83
Q

brain damage sz

A
  • ventricles are larger than those w/o
  • prefrontal cortex smaller than those w/o
  • suspected to occur prenatally
84
Q

onset sz symptoms

A
  • typically between 20-30 yrs old
  • pre-existing prenatal stress
  • post adolescent apoptosis results in complete use prefrontal cortex
  • don’t rely on prefrontal cortex until 21ish
  • when need PFC, psychosis due to prenatal stress starts to appear
85
Q

dopamine hypothesis

A
  • anti-psychotic drugs block dopamine
  • Parkinson’s is due to breakdown of dopaminergic cells
  • if you turn down dopamine, you get parkinson’s and you turn down psychotic symptoms
  • Maybe psychotic symptoms are excess of dopamine
86
Q

anti-psychotic drugs

A
  • haldol- dopamine antagonist that binds to dopamine receptors and doesn’t activate, but blocks
  • some people that take anti-psychotic drugs get Parkinson’s
87
Q

cocaine

A
  • amphtamine
  • dopamine agonist that turns up dopamine concentration
  • sz common in cocaine useres b/c sz characterized by excess of dopamine
88
Q

cerebro-vascular incident

A
  • stroke
  • caused by ischemia and hemorrhage
  • downstream neurons don’t get glucose and oxygen b/c of lack of blood
  • damage/dead downstream neurons
  • Na/K pump slowed down
89
Q

ischemia

A
  • blockage due to something in your blood vessel
90
Q

hemorrhage

A
  • hole in blood vessel
  • blood leaks out
91
Q

therapy for damaged neurons resulting from stroke

A
  • can’t do anything about the dead cells
  • is possible to reabilitate damaged cells
  • in damaged Na/K pump is slowed down
  • need to reabilitate penumbra cells before they become umbra cells
  • have to keep Na+ from building
  • have to stop glial cells
92
Q

Penumbra

A
  • damaged cells near dead cells
  • need to be reabilitated after stroke
93
Q

slow down of Na/K pump

A
  • result of stroke
  • not helped by glial cells
  • Na+ builds up inside cell, leading to over excitation and necrosis
  • penumbra cells -> umbra cells (dead)
94
Q

glial cells and stroke

A
  • release glutamate
  • glutamate is excitatory, so opens Na+ channels
  • not good since the Na/K pump is not working
  • Na+ builds up inside cell -> necrosis
95
Q

why can’t just depress penumbra cells with downer

A
  • only opens Cl- channels
  • doesn’t do anything about Na+
96
Q

hypothermia therapy penumbra cell

A
  • increased temp -> faster reaction
  • turn down brain temp -> slow glial cell release of glutamate -> not as much sodium build up -> ATP pump has time to catch up
  • have to be unconscious
  • lower brain temp reduces destruction of brain tissue following stroke
  • reduces excitement
  • can’t help necrotic cells
97
Q

diachisis

A
  • sudden loss of brain activity
  • stroke damage leads to less overall brain activity
  • immediate stimulant treatment is bad
  • heat and chemical stimulants (glutamate) are BAD for penumbra cells
98
Q

stimulant and stroke

A
  • bad immediately after stroke b/c causes abundance of Na, which cant be removed effectively by Na/K pump (slow)
  • best a few days after stroke
99
Q

what kind of stroke did Cleo suffer from

A
  • hemorrhage
100
Q

traditional first aid for stroke

A
  • place victim under a blanket and keep them warm
  • worst thing to do b/c heat speeds up brain reactions
  • didn’t have meds then
  • blanket was to distract person treating victim
101
Q

cortical plasticity

A
  • cant regenerate new neurons
  • take existing neurons and modify/improve connections
102
Q

phantom limb in past

A
  • Lord Nelson thought was proof of his soul when he lost his arm
  • explanations were hysteria and wishful thinking
  • theroy of frayed (sloppy) nerve endings from battlefield surgery in civil war
103
Q

phantom limb presently

A
  • frayed nerve endings not cause- proved by cleaning up amputations and no change in sensation
  • problem due to brain functions
104
Q

primary somatosensory cortex (S1)

A
  • every spots is a “map” for a place on the body
  • discovered by Wilder Penfield
105
Q

Penfield’s epilepsy experiment

A
  • electrode in somatosensory cortex
  • patient is awake for verbal response
  • applies current to different places
  • finds the spot where the patient feels tingling before seizure
  • removes cells responsible for seizures
106
Q

epilepsy

A
  • brain disorder characterized by seizures
  • synchronous neural firing
  • abnormal electrical activity in brain
107
Q

sever monkey’s sensory nerve

A
  • cut sensory nerve, but leave motor nerve in tact
  • even though motor nerve is fine, monkey treats arm like it is dead
  • when record in somatosensory cortex corresponding to arm, don’t get activity if touch arm, but get activity when stroke cheek
  • Arm activity when face touched
108
Q

Ramachandran

A
  • stroked cheek of motorcycler that lost his arm
  • said feels like stroking cheek AND finger
  • makes sense b/c somatosensory cortex map shows discontinuity between head and hand
  • face connection reorganized to hand in somatosensory
109
Q

relieve phantom pain Ramachandran

A
  • relief for left arm phantom pain
  • use mirror
  • put right arm in spot where feels like left arm is
  • patient feels relief
110
Q

commonsensical notion of memory

A
  • I remember…
111
Q

episodic memory

A
  • memory of event
112
Q

semantic memory

A
  • factual memory
  • word meanings
113
Q

explicit memory

A
  • long term memories
  • kinds that you can describe in words
  • memory of experiences and information
  • conscious
  • Ex: stating that someone is a drunk
114
Q

implicit memory

A
  • unconscious memory
  • previous experiences aid in performance of a task
  • conditioning memories (fear or sensorimotor)
  • skill memories
115
Q

epileptic focus

A
  • where/when seizure occurs
  • touch, smell, feeling, etc
116
Q

bilateral medial temporal lobectomy

A
  • H.M’s procedure for seizures
  • tissue cut and removed
  • post-operative success- IQ increase
  • long term amnesia
  • can make conditioning memories
  • appears he lost hippocampi memories
117
Q

long-term amnesia

A
  • H.M’s situation
  • can’t make new memories- episodic or semantic
  • new people, words, agining appearance, etc
118
Q

classical conditioning

A
  • Pavlov and dogs drooling (unconditioned response) when sees meat (unconditioned stimulus)
  • Bell (neutral stimulus) preceding meat causes drooling
  • dog associates bell with meat
  • bell alone -> drool (conditioned response): bell is no longer neutral b/c dog conditioned to stimulus
119
Q

fear conditioning

A
  • Edouard Claparede
  • patient shakes hands with doc every time he walks in b/c doesn’t remember him
  • one day doc walks in with pin in his hand
  • patient refuses to shake his hand next time
  • doc’s face now associated with pain
  • doc face is conditioned stimulus and fear is conditioned response
  • seems like she can make new memories if associated with fear (would’ve worked for H.M)
120
Q

pain

A
  • unconditioned stimulus
  • fear is the unconditioned response
121
Q

sensorimotor conditioning in H.M

A
  • tone -> puff -> blink
122
Q

eye doctor and conditioning

A
  • puff of air- unconditioned stimulus
  • blink- unconditioned response
  • tone -> puff -> blink
  • tone becomes conditioned stimulus and blink is conditioned response
123
Q

Brenda Miller

A
  • mirror drawing
  • showed H.M a star with a road around it
  • told H.M to take pen and follow the road w/o looking at the star (can only see star in mirror)
  • ability judged by # mistakes
  • begins poorly, but improves with practice
  • H.M can’t remember the experiences of practice, so can’t explain why he can do it
  • implicit memory of skill
124
Q

Morris water maze

A
  • island in pool but can’t see b/c water is murkey
  • uninjured rat can swim and find island and then find it quickly upon next trial
  • rat with hipocampal lesion cannot find island easily next time around
  • hippocampus plays a role in mapping/navigation
125
Q

London cabs

A
  • cab drivers have massive hippocampi
  • as driving experience increases there is a linear increase in hippocampus size
  • exercise hippocampus -> gets bigger
126
Q

H. M and the hippocampus

A
  • forced us to reconsider what memory means
  • short term memory in tact
  • explicit long term memory broken
  • has 2 yrs of retrograde amnesia
  • has majority of anterograde amnesia
  • recall of both explicit and implicit in tack
  • implicit stroage in tact (fear, blink, mirror)
  • CAN’T recall any explicit after surgery
127
Q

amnesia

A
  • no memory
128
Q

memory

A
  • short or long term (test w/ 7 digit recall)
129
Q

long term memory storage and recall

A
  • long term- explicit and implicit
  • memories are stored, but some are not recalled
  • degree of brain trauma determines how much is lost
  • takes a much as 2 hours to move things into long term memory
130
Q

retrograde amnesia

A
  • can’t remember past
  • H.M’s is diffuse (can’t remember from 25-27)
  • playback broken
131
Q

anterograde amnesia

A
  • don’t store forward (new) memories
  • record button broken
132
Q

8 kinds of memory

A
  • explicit storage
  • explicit recall
  • implicit conditioning fear (recall and retrieval)- hand shake
  • implicit conditioning sensorimotor (recall and retrieval)- blink test
  • implicit memory skill (recall and retrieval)- mirror
133
Q

Why did Brenda Milner ask H.M. to learn mirrior-drawing

A
  • proves that he can learn a new skill
  • something he has never done before
  • shows that he has implicit in tact
134
Q

fear conditioning

A
  • Skinner box for classical conditioning
  • warn rat with tone before zapping feet
  • after learning tone rat shows fear to hearing it
135
Q

Joseph LeDoux

A
  • studied conditioning in rats- looking for location of “fear” memory
  • cut out part of rat brain after fear conditioning it
  • decorticated, thalamotomized, and amygdalized
136
Q

hearing sense

A
  • ears -> thalamus -> auditory cortex
137
Q

decorticate out rat’s auditory cortex

A
  • LeDoux cut out auditory cortex
  • profoundly deaf rat
  • play tone
  • still get fear response
  • Interpretation: fear memory must not be in auditory cortex
138
Q

thalamotomized rat

A
  • LeDoux cuts out thalamus
  • play tone
  • fear response abolished
  • Interpretation: thalamus can’t store memories, so fear response stored in thalamus projection location (amygdala)
139
Q

amygdalized rat

A
  • not deaf
  • in tact thalamus and auditory cortex
  • plays tone
  • fear response abolished
  • Interpretation: amygdala stores fear memories
140
Q

two ways to amygdala

A
  • thalamus to amygdala (fast response- low road)
  • auditory cortex to amygdala (slow response- high road)
  • amygdala then instigates behaviors based on emotion (Ex: rat hunkering down in response to fear)
141
Q

why afraid when underwater

A
  • natural response is to clear airway
  • thats why you move frantically and breathe out
  • cortex knows you’re alright (slow road), but amygdala is quick to overreact
142
Q

overactive low road

A
  • panic
  • thalamus to amygdala
  • intuitive system
  • fast, but rough
143
Q

overactive high road

A
  • cortex to amygdala
  • “chocking”
  • overthinking
  • deliberative system
  • slow, but flexible
144
Q

intuitive system

A
  • thalamus to amygdala
  • fast, but rough
145
Q

deliberative system

A
  • cortext to amygdala
  • fast, but flexible
146
Q

H.M memory

A
  • long term implicit in tact
  • long term explicit not in tact
  • skill learning is in tact (implicit)
  • fear learing is in tact (implicit)
  • sensory motor in tact (implicit)
147
Q

acquisition

A
  • acquire an association between neutral stimulus and unconditioned stimulus
  • Ex: tone with puff causes blink
148
Q

extinction

A
  • break connection
  • after learning repeatedly present neutral stimulus w/o unconditioned stimulus
  • Ex: play tone repeatedly w/o puff of air
149
Q

fear conditioning acquisition

A
  • fast
150
Q

fear conditioning extinction

A
  • slow
151
Q

sensorimotor conditioning acquisition

A
  • relatively slow
  • stimulus is less dangerous
152
Q

sensorimotor conditioning extinction

A
  • fast
153
Q

sensorimotor vs fear conditioning

A
  • different behaviors and physiology
  • fear in amygdala
  • sensorimotor in cerebellum
154
Q

Richard Thompson

A
  • tried to identify location of sensorimotor conditioning
  • taught bunny to blink after tone (sensorimotor conditioning)
  • chilled bunny cerebellum -> turn down
  • inject GABA into cerebellum -> turn down
  • bunny isn’t harmed b/c chilling and GABA reversible
  • after chill or GABA, bunny no longer blinks after tone
  • after chill or GABA reversed (recovers), tone association is recovered
155
Q

how are fear and sensorimotor conditioning distinct

A
  • quicker to pick up and slower to distinguish fear conditioning
  • differences physiologically (amygdala vs. cerebellum)
156
Q

what is physiological substate of panic

A
  • overactive low road to amygdala
  • quick responses that aren’t flexible
  • overactive high road to amygdala is choking
157
Q

Lashley and maze learning

A
  • wanted to find out where old memories were b/c H.M had old explicit memories
  • rat motivated by food to find his way through the maze
  • rat makes fewer mistakes every time going through maze
  • like the rat has map of maze in head
  • Lashley cut a particular chunk out of each rat’s cortex
  • Rats still didn’t make any mistakes after cuts, regardless of location
  • Conclusion: effect of cut location means nothing, but size of cut influences performance
158
Q

effects of cut size

A
  • bigger cut results in a more blurred memory
  • still have all memories, they are just blurry
  • memories are like recipes, not blueprints
  • forget butter, cake is still cake, just blurred
  • if you cut out bluprint, something is missing
159
Q

Morris water maze vs Lashley maze

A
  • M: brain damage before learning
  • M: fast trial in maze
  • M: damaged rats in 2nd trial, wander like it was 1st trial
  • M: no damage rats in 2nd trial- find island instantly
  • M: damage to hippocampus
  • M: damage precedes and abolishes learning
  • L: brain damage after learning
  • L: different locations and sizes of damage (cut lateral temporally)
  • L: damage to lateral temporal after learning does NOT abolish learning
  • Conclusion: memories are stored in lateral temporal, they are just smeared across
160
Q

working memory

A
  • kind of like short term memory
  • enables us to organize and control thoughts
  • flexibly respond to changing conditions
  • maintainance of a goal and ability to achieve it
161
Q

Phineas Gage

A
  • metal rod went through skull between optic nerves and removed with no problem
  • vision, thinking, perception, language all fine
  • personality changed
  • lost impulse control (frontal lobe damage)
  • working memory is gone
162
Q

Egas Moniz

A
  • cut out frontal cortex of chimps
  • poked at frontal lobe of violent psychotics
  • successful in chaning personality
  • led to the 40,000 lobectomies in US
163
Q

transorbital frontal lobotomy

A
  • ice pick through eye to brain
  • Egas Moniz
  • success
  • resulted in pleasant psychotics
  • lose who you are and your will
164
Q

Wisconsin card sorting

A
  • assessing frontal lobe syndrome
  • assesses working memory
  • can sort cards by number, color, or shape
165
Q

Korsakoff’s syndrome

A
  • brain damage in frontal cortex and lateral temporal cortex
  • lateral temporal cortex where old memories are
  • retrograde amnesia and impulse control gone
166
Q

confabulation

A
  • making things up
  • and believing it b/c don’t have any old memories to make you think otherwise
  • characteristic of Korsakoff’s syndrome
167
Q

timecourse for retrograde amnesia for H.M

A
  • 2 years
  • tells us hippocampus holds memories for 2 yrs
168
Q

timecourse retrograde amnesia following ECT

A
  • 2 hours
  • takes about 2 hours to make memories solid
169
Q

retrograde amnesia for Korsakoff sufferers

A
  • no limit
  • can go all the way back to child
  • cutting out ALL memories

Physiological Psychology (7 decks)

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