Chapter 13: The Biology of Learning and Memory Flashcards

1
Q

Classical Conditioning

A

-pairing two stimuli changes the response to one of them
-Pavlov’s dog
CS+UCS=UCR (initially)
Bell + Meat = Salivation
CS -> CR
Bell -> Salivation

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2
Q

Operant/Instrumental Conditioning

A

-individual’s response leads to reinforcement (increases future probability of response) or punishment (decreases frequency of response)

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3
Q

describe Lashley’s search for the engram

A
  • Lashley reasoned that if learning depends on new or strengthened connections between 2 brain areas a knife cut somewhere in the brain should interrupt that connection and abolish learned response
  • no knife cut significantly impaired learning
  • also found lesions impaired performance but deficit depended more on amount of damage than location
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4
Q

engram

A
  • physical representation of what has been learned

ex) connection between 2 brain areas

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5
Q

Lashley’s 2 principles

A

equipotentially- all parts of cortex contribute equally to complex behaviours such as learning and any part of the cortex can substitute for any other
mass action- cortex works better as a whole and more cortex is better

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6
Q

2 Unnecessary assumptions for Lashley’s findings

A

1) cerebral cortex or only place to search for engram

2) all kind of memory are physiologically the same

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7
Q

Richard Thompson

A
  • studied classical conditioning of eyelid response in rabbits
  • LIP (lateral interpositus nucleus) essential for learning
  • when LIP was suppressed learning had no effects
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8
Q

characteristics of short-term memory

A
  • maximum capacity
  • depends on rehearsal
  • forget something=lost forever
  • emotionally significant memories form quicker
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9
Q

characteristics of long-term

A
  • vast difficulties to estimate capacity
  • can recall long term memories you haven’t thought about in years
  • hint can help reconstruct something you thought you forgot
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10
Q

characteristics of working memory

A
  • way we store info while we are working with it
  • test=delayed response task
  • older people have impairments of working memory due to changes in prefrontal cortex
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11
Q

describe the theories of the function of the hippocampus in declarative memory, spatial memory, context learning, and consolidation

A

-

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12
Q

Declarative memory

A
  • hippocampus is critical for declarative memory (especially episodic)
  • hippocampal damage impairs delayed matching and nonmatching to sample task (remembering object that was present in an occasion)
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13
Q

Spatial Memory

A
  • when people perform spatial tasks fMRI results show enhanced activity in hippocampus (visualizing a route from one place to another)
  • MRI scans showed taxi drivers have larger than average posterior hippocampus (directly proportional to length of time as taxi driver)
  • shows growth of hippocampus in response to spatial learning activities
  • maze activities- people/rats with damage have trouble remembering where they have already been
  • species comparisons show link between hippocampus and spatial memory
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14
Q

Contextual memory

A

Hippcampus-important for remembering details and includes lots of detail, as time passes memory becomes less detailed and more dependent on cerebral cortex

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15
Q

Consolidation

A
  • small to moderate amounts of cortisol activate amygdala and hippocampus where they enhance storage and consolidation of recent experiences
  • amygdala in turn stimulates hippocampus and cerebral cortex (both important for memory storage)
  • prolonged stress (increase cortisol) impairs memory
  • consolidation can be fast or slow and depends on more than time necessary to synthesize new proteins
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16
Q

causes of Korsakoff’s syndrome

A

Cause-

  • brain damages caused by prolonged thiamine deficiency
  • chronic alcoholic
  • deficiency leads to loss of shrinkage or neurons in brain
17
Q

Most affected brain area in Korsakoff’s syndrome

A

-most affected area=dorsomedial thalamus

18
Q

Symptoms of Korsakoff’s syndrome

A
  • apathy, confusion, memory loss

- distinctive symptom=confabulation (mainly for episodic memory questions)

19
Q

Alzheimer’s Disease

A
  • better procedural than declarative memory
  • memory and alertness vary substantially suggesting problems results from malfunctioning neurons rather than neuron death
  • gradually progresses to more serious memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, loss of appetite
20
Q

Genetic link to Alzheimer’s

A
  • gene on chromosome 21 linked with Alzheimer’s

- genes to not completely control

21
Q

Early onset Alzheimer’s damage

A
  • causes protein Amyloid-B to build up inside and outside neurons
  • damage varies but net effect=damage to dendritic spine , decrease synaptic input and decreased plasticity
  • damage from amyloid clusters into plaques
  • plaque accumulate- in cerebral cortex, hippocampus and other areas atrophy
22
Q

Tau protein and Alzheimer’s

A

-becomes altered with more phosphate groups causing them not to be able to bind with usual targets within axons and results in spreading to cell body and dendrites=magnifies damage

23
Q

other brain areas that contribute to various aspects of memory

A
  • gradual learning depends on basal ganglia (implicit or abit learning)
    ex) what a basketball player on another team is most likely to do in a situation so you can guard better
24
Q

Basal ganglia contribute to memory

A

-important for procedural memory

25
Q

Parietal lobe damage and memory

A

-process of associating one piece with another is impaired

26
Q

damage to anterior and inferior temporal lobe and memory

A

-semantic dementia (trouble remembering specific words)

27
Q

mechanisms of habituation and sensitization in Aplysia

A

-marine invertebrate related to common slug that has larger and fewer neurons that are easier to study

28
Q

habituation Aplysia

A
  • decrease in response to a stimulus that is presented repeatedly accompanied by no other change in other stimuli
    ex) repeated stimulation of aplysia gills with brief jet of seawater it withdraws at first but after multiple reps it stops responding
  • > not due to muscle fatigue
  • > not due to change in sensory neuron
    conclusion: habituation depends on change in synapse between sensory neuron and motor neuron
29
Q

sensitization Aplysia

A
  • increase in response to mild stimuli as results of exposure to more intense stimuli
    ex) strong stimulus almost anywhere on Aplysia skin intensifies a later withdraw/response to touch
  • how this happens (p. 412)
30
Q

describe the characteristics of long-term potentiation (LTP)

A
  • 1+ axons connected to dendrite bombard it with rapid series of stimuli
  • burst of intense stimulation leaves some of the synapses potentiated (more responsive to new input of same type) for minutes, days, weeks
31
Q

Properties of LTP

A

1) Specificity- only active cells become strengthened
2) Cooperativity- nearly simultaneous stimulation 2+ axons produces LTP much more strongly than does repeated stimulation by 1 axon
3) Associativity- pairing weak input with strong input enhances later response to weak input

32
Q

LTD (long term depression)

A
  • prolonged decrease in response at synapse occurs for axons that have been less active than others
  • 1 synapse strengthens another weakens
33
Q

roles of AMPA and NMDA receptors in LTP

A
  • entry of Ca2+=key to maintaining LTP

- maintaining of LTP also depends on CaMKII, CREB, BDNF forming

34
Q

AMPA Receptor

A
  • excited by glutamate and AMPA

- Na+ channels opened by receptor

35
Q

NMDA receptor

A
  • ordinarily excited by glutamate but can respond to drug NMDA
  • depends on degree of polarization across the membrane NMDA channel opens only if Mg2+ leaves (depolarize membrane decreases negative charge that attracts it)
36
Q

AMPA and NMDA receptors

A

-ionotropic receptors (stimulated open a channel to let ions enter post-synaptic cell)

37
Q

Final outcome varies including

A
  • dendrite builds more AMPA receptors or moves old ones to better positions
  • dendrite may make more branches and spines thus forming additional synapses with same axon
  • phosphate groups attach to certain AMPA receptors to make them more responsive than before
  • neurons make more NMDA receptors