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Learning and Memory Flashcards

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1
Q

Who was classical conditioning pioneered by?

A

Ivan Pavlov.

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2
Q

What is the basis of classical conditioning?

A

Pairing two stimuli changes the response to one of them.

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3
Q

Explain operant conditioning.

A

The individuals response followed by a reinforcer or punishment.

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4
Q

What are reinforcers?

A

Events that increase the probability that the response will occur again.

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5
Q

What is punishment?

A

Events that decrease the probability that the response will occur again.

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6
Q

What is an engram?

A

A physical representation of what had been learned.

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7
Q

Who searched for the engram?

A

Lashley.

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8
Q

What did Lashley’s experiments show?

A

Learning and memory do not rely on a single cortical area.

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9
Q

Name Lashley’s principles about the nervous system.

A

Equipotentiality, and mass action.

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10
Q

Explain equipotentiality.

A

All parts of the cortex contribute equally to complex functioning behaviours.

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11
Q

Explain mass action.

A

The cortex works as a whole, and more cortex is better.

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12
Q

Where is the classical conditioning engram located?

A

The cerebellum, not the cortex.

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13
Q

Who discovered the classical conditioning engram?

A

Thompson.

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14
Q

What is the lateral interpositus nucleus (LIP) identified as central for?

A

Learning.

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15
Q

What are Hebb’s two types of memory?

A

Short-term memory, and long-term memory.

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16
Q

Give three differences between short and long-term memory.

A

Short-term memory has a limited capacity, and fades quickly, and long-term memories can be stimulated with a cue.

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17
Q

What enhances the consolidation of recent experiences?

A

Epinephrine and cortisol.

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18
Q

Who proposed working memory?

A

Baddeley and Hitch.

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19
Q

What is working memory?

A

An alternative short-term memory.

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20
Q

What is the emphasis of working memory?

A

Temporary storage of information to actively attend to it and work on it for a period of time.

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21
Q

What is the common test of working memory?

A

The delayed response task.

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22
Q

What does the delayed response task involve?

A

Requires responding to something you heard or saw a short while ago.

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23
Q

Where is working information stored?

A

The prefrontal cortex.

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24
Q

What is vital for the formation of new long-term memories?

A

Hippocampus.

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25
Q

What are the two major types of amnesia?

A

Anterograde amnesia, and retrograde amnesia.

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26
Q

Explain anterograde amnesia.

A

Loss of ability to form new memory after the brain damage.

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27
Q

Explain retrograde amnesia.

A

Loss of memory of events prior to the occurrence of the brain damage.

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28
Q

Explain semantic memory.

A

Memories of factual information.

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29
Q

Explain episodic memory.

A

Memories of single personal events.

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30
Q

What is explicit memory?

A

Deliberate recall of information that one recognises as a memory.

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31
Q

What is implicit memory?

A

The influence of experience on behaviours even if one does not recognise that influence.

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32
Q

What is procedural memory?

A

A special kind of implicit memory, development of motor skills and habits.

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33
Q

Give five characteristics of amnesia patients.

A

Normal working memory, unless distracted, severe anterograde amnesia, severe loss of episodic memories, better implicit than explicit memory, and nearly intact procedural memory.

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34
Q

What two tasks does damage to the hippocampus impair?

A

Radial mazes and the Morris water maze task.

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35
Q

What is a radial maze task?

A

A subject must navigate a maze that ha eight or more arms with a reinforcer at the end.

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36
Q

What is a Morris water maze task?

A

A rat must swim through murky water to find a rest platform just underneath the surface.

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37
Q

What is Korsakoff’s syndrome?

A

Brain damage caused by prolonged thiamine (vitamine B1) deficiency.

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38
Q

What does Korsakoff’s syndrome cause?

A

It impedes the brain’s ability to metabolise glucose, leading to a loss of or shrinkage of neurons in the brain.

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39
Q

What are some characteristics of Korsakoff’s syndrome?

A

Confabulation (taking guesses to fill in gaps in memory), confusion, and memory loss.

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40
Q

Alzheimer’s disease is associated with an accumulation and clumping of:

A

Amyloid beta protein, and an abnormal form of the tau protein.

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41
Q

What does the amyloid beta protein do?

A

Produces widespread atrophy of the cerebral cortex, hippocampus and other areas.

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42
Q

What is the abnormal form of the tau protein?

A

Part of the intracellular support system of neurons.

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43
Q

Accumulation of the amyloid beta and tau proteins results in:

A

Plaques and tangles.

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44
Q

What are plaques?

A

Structures formed from damaged axons and dendrites.

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45
Q

What are tangles?

A

Structure formed from degeneration within neurons.

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46
Q

Which brain area does gradual learning rely on?

A

The basal ganglia.

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47
Q

What kind of learning is the amygdala associated with?

A

Fear learning.

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48
Q

Which brain area pieces information together?

A

The parietal lobe.

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49
Q

What does damage to the anterior temporal cortex result in?

A

A loss of semantic memory.

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50
Q

Which brain area is involved in learned behaviour and decision-making.

A

The prefrontal cortex.

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51
Q

What is the Hebbian synapse?

A

A synapse that increases in effectiveness because of simultaneous activity in the presynaptic and postsynaptic neurons.

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52
Q

What kind of synapse may be critical for many kinds of associative learning?

A

Hebbian synapses.

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53
Q

When does long-term potentiation (LTP) occur?

A

When one or more axons bombard a dendrite with stimulation.

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54
Q

What is the result of long-term potentiation (LTP)?

A

It leaves a synapse potentiated for a period of time and the neuron is more responsive.

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55
Q

Explain long-term depression (LTD).

A

A prolonged decrease in response at a synapse that occurs when axons have been less active than others.

56
Q

What is the compensatory process?

A

As one synapse strengthens, another weakens.

57
Q

What does LTP depend on?

A

Changes at glutamate receptors.

58
Q

Name two types of glutamate receptors.

A

AMPA receptors, and NMDA receptors.

59
Q

What does repeated glutamate excitation of AMPA receptors do?

A

Depolarise the membrane.

60
Q

What does depolarisation of AMPA receptors displace?

A

Magnesium molecules that had been locking NMDA receptor.

61
Q

What happens after the NMDA receptors are exposed?

A

Glutamate excites them, opening a channel for calcium ions to enter the neuron.

62
Q

What does calcium entry through the NMDA channel result in?

A

Activation of a protein, which alters the make-up of the cell.

63
Q

What does protein activation of NMDA receptors cause? (3)

A

More AMPA receptors being built and increased dendritic branching, and increased future responsiveness to glutamate.

64
Q

What does release of a retrograde transmitter back to the presynaptic cell trigger? (2)

A

Increased neurotransmitter release, and transmitter release from additional sites.

65
Q

How do caffeine and ritalin enhance learning?

A

By increasing arousal.

66
Q

How is a conditioned response developed?

A

A conditioned stimulus and unconditioned stimulus are presented multiple times, until the individual begins making a new, learned response to the conditioned stimulus.

67
Q

What is an unconditioned response?

A

Where presentation of the conditioned stimulus and unconditioned stimulus has no effect on the individual.

68
Q

Explain instrumental conditioning.

A

An individual’s response leads to a reinforcer or punishment.

69
Q

What is the primary difference between classical and instrumental conditioning?

A

In instrumental conditioning the individual’s response determines the outcomes, while in classical conditioning the CS and UCS occur at certain times regardless of the individual’s behaviour.

70
Q

What two assumptions do Lashley’s conclusions rest on that have no grounds?

A

That the cerebral cortex is the best or only place to search for an engram, and that studying one example of learning is just as good as studying any other one.

71
Q

What it is equipotentiality?

A

All parts of the cortex contribute equally to complex behaviours like learning, and any part of the cortex can substitute for any other.

72
Q

What is mass action?

A

The cortex works as a whole, and more cortex is better.

73
Q

Where did Thompson search for the engram?

A

The cerebellum.

74
Q

What did Thompson identify as integral to learning?

A

The lateral interpositus nucleus (LIP).

75
Q

What did Hebb believe regarding learning?

A

No one mechanism could account for all the phenomena of learning.

76
Q

What did Hebb propose in regards to memory?

A

Short-term memory and long-term memory.

77
Q

What evidence supports Hebb’s theory?

A

Short and long-term memory differ in capacity, short-term memory depends on rehearsal, and long-term memory can be prompted.

78
Q

Where did Hebb think short-term memories were stored?

A

In a reverberating circuit.

79
Q

What was Hebb’s view on consolidation?

A

If something was held in short-term memory for log enough, the brain might consolidate it into long-term memory.

80
Q

How are emotionally significant memories formed quickly?

A

Epinephrine and cortisol activate the amygdala and hippocampus, where they enhance the storage and consolidation of recent experiences.

81
Q

How does the amygdala aid memory storage?

A

It stimulates the hippocampus and cerebral cortex, which are both important for memory storage.

82
Q

Who introduced the concept of working memory?

A

Baddeley and Hitch.

83
Q

What is a common test of working memory?

A

Delayed response task.

84
Q

What occurs in the brain during the delay in a delayed response task? (2)

A

Prefrontal and parietal cells increase their activity, and different cells become active depending on the direction eye movement will need to take.

85
Q

What occurs in the brain during visual working memory?

A

Cells in the prefrontal cortex synchronise activity with other cortical areas.

86
Q

Explain anterograde amnesia.

A

An inability to form memories that happened after brain damage.

87
Q

Explain retrograde amnesia.

A

A loss of memory for events that occurred before the brain damage.

88
Q

What are semantic memories?

A

Memories of factual information.

89
Q

What is episodic memory?

A

Memories of single personal events.

90
Q

What is explicit memory?

A

Deliberate recall of information that one recognises as a memory.

91
Q

Give another name for explicit memory.

A

Declarative memory.

92
Q

What is implicit memory?

A

An influence of experience on behaviour, even if you do not recognise that influence.

93
Q

Explain procedural memory.

A

The development of motor skills and habits.

94
Q

What kind of memory is procedural memory?

A

Implicit memory.

95
Q

Who proposed that the hippocampus is critical for declarative memory?

A

Squire.

96
Q

Explain the delayed matching-to-sample task.

A

An animal sees an object and then, after a delay, gets a choice between two objects, from which it must choose the one that matches the sample.

97
Q

Explain the delayed nonmatching-to-sample task.

A

The procedure is the same except that the animal must choose the object that is different from the sample.

98
Q

What are the delayed matching-to-sample task and the delayed nonmatching-to-sample task tests of?

A

Episodic or declarative memory.

99
Q

What is acute transient global amnesia?

A

A rare condition where people have a temporary dysfunction of the hippocampus.

100
Q

What happens in the brain when people recall an episodic memory?

A

Activity in and around the hippocampus synchronises which activity in other parts in the cortex.

101
Q

What do memories with less contextual detail depend on?

A

The hippocampus.

102
Q

What do older less detailed memories rely on?

A

The cerebral cortex.

103
Q

When does severe thiamine deficiency occur?

A

In chronic alcoholism where drinkers go for weeks at a time on a diet of nothing but alcohol, lacking in vitamins.

104
Q

Why does the brain need thiamine?

A

To metabolise glucose, its primary fuel.

105
Q

What does prolonged thiamine deficiency lead to?

A

A loss of shrinkage of neurons throughout the brain.

106
Q

What area is most affected by thiamine deficiency and what does this cause?

A

The dorsomedial thalamus, the main source of input to the prefrontal cortex.

107
Q

Give some symptoms of Korsakoff’s syndrome.

A

Apathy, confusion and memory loss, as well as major impairment of episodic memory but sparing of implicit memory.

108
Q

What is the most distinctive symptom of Korsakoff’s syndrome?

A

Confabulation, filling in memory gaps with guesses.

109
Q

What kind of memory is best in Alzheimer’s patients?

A

Procedural rather than declarative.

110
Q

What are the symptoms of progressive Alzheimer’s disease?

A

Serious memory loss, confusion, depression, restlessness, hallucinations, delusions, sleeplessness, and loss of appetite.

111
Q

How many people does Alzheimer’s affect between the ages of 65-74?

A

5%

112
Q

How many people does Alzheimer’s affect over 85?

A

50%

113
Q

What gene is linked to early-onset Alzheimer’s disease?

A

Chromosome 21.

114
Q

What protein do genes producing early-onset Alzheimer’s produce, and what are the effects of it?

A

Amyloid-B, which accumulates both outside and inside neurons, causing damaged dendritic spines, decreased synaptic input, and decreased plasticity.

115
Q

As amyloid damages axons and dendrites, the damaged structures cluster into structures called:

A

Plaques.

116
Q

As plaques accumulate:

A

The cerebral cortex, hippocampus and other areas atrophy.`

117
Q

What causes tangles?

A

An altered tau protein.

118
Q

How does the basal ganglia integrate information?

A

Gradually, over many trials.

119
Q

How quickly can the hippocampus and cerebral cortex learn?

A

In one trial.

120
Q

How does the basal ganglia learn?

A

Through immediate feedback.

121
Q

How do the cerebral cortex and hippocampus learn?

A

Through connecting information over time and through delayed feedback.

122
Q

What is the effect of damage to the basal ganglia?

A

Loss of well-learned motor patterns, and impaired learning of skills and habits.

123
Q

What is the effect of damage to the cerebral cortex and hippocampus?

A

Impaired declarative memory, especially episodic.

124
Q

What is semantic dementia?

A

Damage to the anterior temporal cortex causing a loss of semantic memory.

125
Q

What is the ventral prefrontal cortex important for?

A

Learning about rewards and punishments and making decisions based on them.

126
Q

Explain a Hebbian synapse.

A

A synapse that increases in effectiveness because of simultaneous activity in the pre and postsynaptic neurons.

127
Q

Explain habituation.

A

A decrease in response to a stimulus that is presented repeatedly and accompanied by no change in other stimuli.

128
Q

Explain sensitisation.

A

An increase in response to mild stimuli as a result of exposure to more intense stimuli.

129
Q

What excites a facilitating interneuron?

A

Strong stimulation on the skin.

130
Q

How does serotonin cause long-term sensitisation?

A

Serotonin blocks potassium channels, resulting in longer repolarisation, so that the preynaptic neuron continues releasing the neurotransmitter for longer than usual.

131
Q

What is long-term potentiation?

A

One or more axons connected to a dendrite bombard it with a rapid series of stimuli, leaving the synapses potentiated for minutes, days, or weeks.

132
Q

Name LTP’s three properties that make it an attractive candidate for a cellular basis of learning and memory.

A

Specificity, cooperativity, and associativity.

133
Q

Explain LTP’s specificity.

A

If some of the synapses onto a cell have been highly active and others have not, only the active ones become strengthened.

134
Q

Explain LTP’s cooperativity.

A

Nearly simultaneous stimulation by two or more axons produced LTP much more strongly than does repeated stimulation by just one axon.

135
Q

Explain LTP’s associativity.

A

Pairing a weak input with a strong input enhances later response to the weak input.

136
Q

What is long-term depression (LTD)?

A

A prolonged decrease in response at a synapse, occurs for axons that have been less active than others.

Physiological Psychology (6 decks)

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