Unit 2 lecture Flashcards
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
*
2
Q
pathway
A
- result of neuromigration during development
3
Q
history (science explanation)
A
- neurosculpting
- start with undifferentiated neurons and then figure out who you are by wiring specific neurons
4
Q
neural wiring
A
- dedicated pathways and history
5
Q
zygote
A
single cell (sperm+egg)
6
Q
embryo
A
- 2 or more cells
- totipotent
7
Q
stem cell
A
- have the potential to differentiate into any cell
- regenerate
8
Q
totipotent
A
- ability of single cell to divide and produce all the differentiated cells that make up an organism
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
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)
11
Q
migration
A
- neron has to migrate to target in spine
- genetics and chemical influences determine migration during development
12
Q
difference between fetus and embryo
A
- fetus at 3 months b/c start looking human
13
Q
how does neuron know where to travel
A
- growth cone serves as “feelers”
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
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
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)
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
18
Q
neurotrophins
A
- enhance growth
- Ex: nerve growth factors
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
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
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
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
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
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
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
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
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
28
Q
frontal cortex
A
identity
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
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
31
Q
how does neuron find its target
A
chemicals
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
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
34
Q
what are 3 epochos characterized by massive apoptosis
A
- ) prenatal- before birth
- ) paranatal- after birth
- ) age 21- find identity then other connections not used die
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
36
Q
turpsichore
A
- goddess of dance
- chorea from Huntington’s chorea
37
Q
Huntington’s chorea
A
- dominant and lethal
- lose inhibitory -> everything you do is excitatory
- always overshoot destination
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
39
Q
homozygous for dominant w/ heterozygous for lethal
A
- no kids express double recessive lethal version
40
Q
Hapsberg
A
- kept mating with each other so more and more prominant jaw
41
Q
mutations
A
- maladaptive
- lethal
- most often recessive
42
Q
arranged marriage where you meet on wedding night
A
- more successful
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
44
Q
arranged marriage with childhood acquaintance
A
- less successful b/c genes don’t like to have sex with closely related
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)
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
47
Q
door w/o spring and shock absorber
A
- spring- excitatory
- shock absorber- inhibitory
- stimulates motor neurons
48
Q
how can lethal gene be dominant
A
- lethal at onset
- lethal genes passed on to kids
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
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
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
52
Q
addictive drug
A
- targets dopamine
- cocaine, alcohol, heroin, etc
- Marijuana and LSD NOT addictive
53
Q
dopamine action
A
- ) dopamine release
- ) dopamine transporter release
- ) dopamine & transporter to soma
- ) in soma dopamine removed and recycled (repackaged)
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
55
Q
MPTP and dopamine transporter
A
- high affinity
- blocks up mitochondria
- cell can’t function w/o mitochondria
- dopaminergic cell dies
56
Q
treat parkinson’s
A
- L-dopa
- stem cells
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
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
59
Q
will we all develop parkinson’s
A
yes b/c dopaminergic cells die off over time
60
Q
negative symptoms of schizophrenia (SZ)
A
- lacking something normal people have
- flat affect
- catatonia
- waxy flexibility
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
62
Q
dopamine and substantia nigra
A
- loss of dopaminergic neurons in substantia nigra results in Parkinson’s
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
64
Q
diagnosing sz
A
- negative and positive symptoms
65
Q
positive symptoms sz
A
- have something extra that normal people don’t have
- NOT such a good thing
- psychotic cluster
- disorganized cluster
66
Q
affect
A
expression of feeling or emotion
67
Q
psychotic cluster
A
- positive symptom sz
- generally expressed by age 30
- hallucinations- generally auditory
- delusions
- paranoia
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
