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Psych 275 > Chapter 14: Learning and Memory > Flashcards

Chapter 14: Learning and Memory Flashcards

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1
Q

What does dyslexia result from? In what area of the brain is it?

A

neuron clusters/warts from birth; reduced activity in the tempo parietal cortex

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2
Q

What is eyeblink conditioning and what part of the brain is active during it?

A

a tone is associated with a puff of air; the cerebellum

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3
Q

What is fear conditioning and what part of the brain is active during it?

A

conditioned emotional response between neutral stimuli and unpleasant events; the amygdala

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4
Q

What is amnesia and what type of tasks do typical amnesia patients perform normal on?

A

the partial or total loss of memory; on implicit memory tasks

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5
Q

What is a learning set?

A

the “rules of the game”, how a problem can be solved in a given situation; is stored in memory

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6
Q

What is priming and what type of memory does it mostly relate to?

A

using a stimulus to sensitize the nervous system to a later presentation of the same or similar stimulus; implicit memory

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7
Q

What lobes are STM and LTM processed in?

A

frontal and temporal lobes respectively

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8
Q

Where are memories for colour stored?

A

the ventral temporal

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9
Q

Where are memories for motion stored?

A

the middle temporal gyrus

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10
Q

Where is episodic memory processed?

A

the frontal lobe but connections in various areas

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11
Q

What is shown in brain scans for those with highly superior AM?

A

an increase in gray matter in the temporal and parietal lobes

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12
Q

What did H.M. have removed? What was the result?

A

hippocampus, amygdala and some surrounding; could not form new explicit memories

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13
Q

Where is implicit motor memory located?

A

in the basal ganglia

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14
Q

What is the neural circuit for explicit memories?

A

major cortical areas both Perirhinal and Parahippocampal entorhinal hippocampus

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15
Q

Where is the entorhinal cortex and what does it do?

A

medial temporal lobe surface; it is the major route for neocortical input to the hippocampal formation; the integrative area

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16
Q

What happens if the entorhinal cortex degenerates?

A

Alzheimers

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17
Q

Where is the parahippocampal cortex and what type of information does it receive and relay?

A

along the dorsal medial temporal lobe surface; visuospatial memory

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18
Q

Where is the perirhinal cortex and what type of info does it receive and relay?

A

next to the rhinal fissure on the ventral surface of the brain; the visual stream

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19
Q

What are 2 possible ways for Alzheimers to develop?

A

1) Loss of cholinergic cells in the basal forebrain

2) Development of neuritic plaques in the cerebral cortex

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20
Q

What are neuritic plaques?

A

dead tissue with a central protein core surrounded by degenerative cell fragments

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21
Q

Where is spatial memory processed?

A

the hippocampus

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22
Q

What types of cells are in the hippocampus to process spatial memory? (3)

A

1) Place cells - certain location
2) Head direction cells - particular direction
3) Grid cells - tells us how big where we are is

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23
Q

What are the reciprocal functions of explicit memory and what is their purpose?

A

1) from the MT to the cortical layers - keeps sensory info alive
2) Back to the neocortex - keeps it appraised? (review this)

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24
Q

What is Korsakoff syndrome and what is it caused by?

A

both retrograde and anterograde amnesia resulting from diencephalic damage because of alcohol use and vitamin B deficiency

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25
Q

Where does consolidation of explicit memories take place?

A

in the hippocampus

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26
Q

What does the basal forebrain help do for explicit memories?

A

maintains activity levels in forebrain areas so that memories can be stored

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27
Q

What is the neural circuit for implicit memories? What is different about it from explicit?

A

sensory and motor info –> neocortex –> basal ganglia (also receives info from substantia nigra) –> ventral thalamus –> premotor cortex ; there is no feedback

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28
Q

What sends and receives info to and from the amygdala in the neural circuit for episodic memories?

A

the medial temporal cortex, basal ganglia and hypothalamus and PAG

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29
Q

Where do the hypothalamus and PAG exchange info with?

A

the amygdala and the frontal, parietal, temporal, occipital and cingulate cortices

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30
Q

What is long-term potentiation?

A

a long-lasting increase in synaptic effectiveness after high-frequency stimulation

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31
Q

What is long-term depression? What is it hypothesized to be a part of?

A

long lasting decrease in synaptic effectiveness after low frequency electrical stimulation; clearing out old memories

32
Q

What is AMPA’s role in the LTP process?

A

it mediates responses when glutamate is released; if enough glutamate is released then it allows Na+ to enter and depolarize

33
Q

What is NMDA blocked by and what does it allow to pass if depolarized?

A

blocked by Mg2+ and allows Ca2+ to pass

34
Q

What are the 2 conditions that must be satisfied for NMDA to open?

A

1) Postsynaptic depolarized (Mg2+ displaced)

2) NMDA receptors activated by glutamate

35
Q

What molecule plays the crucial role in LTP that is moderated by NMDA?

A

Ca2+

36
Q

What effects does Ca2+ have in relation to LTP?

A

1) Increased responsiveness of AMPA
2) Formation of new AMPA receptors
3) Release of more glutamate

37
Q

What is the BrdU technique used to detect?

A

new neurons in the mammalian brain?

38
Q

What qualities of brain did enriched rats have compared to regular?

A

more dendrites, glial cells and blood capillaries; also more neurons in hippocampus and more

39
Q

Where did amputated hand sensors move?

A

to the face –> increased sensitivity/responsiveness to face

40
Q

What is dystonia?

A

a blending of finger representation that messes up hand movements because of overuse as well as vibrations moving through fingers (usually in musicians)

41
Q

What type of people have more dendritic branches in Wernicke’s area?

A

college educated people and females

42
Q

What happens if you block the methylation of DNA in hippocampus?

A

no memory

43
Q

What effect does estrogen levels in women during their cycles have on the brain?

A

increased dendrite spines in the neocortex but less in the hippocampus

44
Q

What do Neurotrophic factors do?

A

signal stem cells to turn in to neurons of glia

45
Q

What does Nerve Growth Factor (NGF) do?

A

stimulates neuron growth and survival?

46
Q

What neurotrophic factor plays a role in learning?

A

BDNF

47
Q

What is drug-induced behavioral sensitization and what types of drugs cause it?

A

escalating behavioral response to repeated administration of a psychomotor stimulant; amphetamine, cocaine, caffeine

48
Q

What does drug induced behavior sensitization do to the brain?

A

increases receptors/synapses in the prefrontal cortex and nucleus accumbens (dopamine areas); stops hinders learning of complex environments later

49
Q

What are the 3 potential recovery solutions to Brain Injury?

A

1) Compensate with out body/brain parts
2) Grow new circuits
3) Lost neuron replacement

50
Q

What does growing new circuits allow the brain to do? What can be done to result in it?

A

do more with less; deep brain stimulation and NGF (promotes growth)

51
Q

What is a growth factor that is used to replace neurons? Where is it and what does it do? What else is needed?

A

epidermal growth factor; in ventricles; stimulates neuron and glia growth in the striata; trophic factors also needed

52
Q

What are 3 things the brain is according to Dickson?

A

1) a sensory-motor integrator
2) dynamic and modifiable
3) a storage device

53
Q

What are the 2 premises of neurobio?

A

1) NS operation is completely responsible for behavior and mind
2) Environmental influences that change/modify behavior must be reflected by functional changes

54
Q

What did Muller and Pilzecker research?

A

rehearsal, consolidation and interference

55
Q

What did William James research?

A

different aspects/types of memory

56
Q

What was a saying that was famously said by Hebb? What was the backing of this?

A

cells that fire together wire together; that there was activity dependent enhancement of synaptic transmission (LTP)

57
Q

Who first researched LTP? What were they studying?

A

Bliss and Lomo; transmission in the hippocampus

58
Q

What are the 3 properties of LTP?

A

1) Cooperativity: threshold aspect of it
2) Associative: associate weak with strong so weak can bring LTP by itself
3) Specificity: LTP expressed only in active synapses and not nearby ones

59
Q

After LTP is induced what is NMDA’s role?

A

it is not needed anymore; only useful for induction

60
Q

What is Calmodulin dependent protein Kinase II? What does it do?

A

it is the “memory molecule” when activated promotes LTP and when inhibited stops LTP

61
Q

What are the 3 phases of LTP?

A

1) Early - Induction: NMDA activation and Ca2+ dependence
2) Medium - expression: changes to receptors and release; local protein synthesis
3) Late - Maintenance: genomic involvement (translation dependent); possible anatomical changes

62
Q

What is significant about the Aplysia’s gill withdrawal reflex? (3)

A

it shows habituation, sensitization and classical conditioning; a monosynaptic connection evokes the reflex; also has interneurons though that are modulatory

63
Q

What happens during habituation to the presynaptic neuron?

A

decrease in width of action potential; less physical connections between neurons

64
Q

What learning process is classical conditioning similar to at the cell level?

A

sensitization

65
Q

What kind of process is required for memory at the cellular level?

A

protein synthesis and perhaps the transcription of DNA-RNA; memory requires gene expression that leads to new proteins

66
Q

Where is the Memory trace located according to Karl Lashley? How did he come to this conclusion?

A

diffusely in the brain; by removing parts of the brain and realizing that it had the property of equipotentiality (parts could take over to do the same tasks

67
Q

What did Ribot discover about amnesia?

A

the loss of memory is inversely related to the closeness to the injury

68
Q

What did patient H.M. have removed and what was the result?

A

the medial temporal lobe (hippocampus, entorhinal cortex, parahippocampal cortex and amygdala) and then he had profound anterograde explicit amnesia but IQ actually increased

69
Q

For a DNMS for rats what lesions were there a notable performance difference? Which weren’t there?

A

MTL noticeable; hippocampus not

70
Q

What part of the brain is responsible for temporally ordering events?

A

the frontal lobe

71
Q

Where is the damage for korsakoff syndrome?

A

medial thalamus and the medial hypothalamus (the medial diencephalon)

72
Q

What lobe is central to long-term explicit memory formation?

A

the temporal lobe

73
Q

What do concussions disrupt? Why?

A

the consolidation process; perhaps because it interferes with frontal lobe action

74
Q

Where does the standard consolidation theory suggest memories are stored temporarily?

A

the hippocampus

75
Q

What is the distributed reinstatement theory?

A

a learning episode rapidly produces a stored memory representation that is strong in the hippocampus but weak elsewhere

Psych 275 (13 decks)

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