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SMP - Neurophysio Exam 2 > Lectures 9 & 10 - Learning and Memory > Flashcards

Lectures 9 & 10 - Learning and Memory Flashcards

1
Q

What is learning?

A

The act of acquiring new or modifying existing knowledge, behaviors, skills, etc.

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2
Q

What is memory?

A

Ability to retain and recall information, skills, etc. and is an enduring change in an organism’s function over time

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3
Q

What are the 3 types of memory?

A
  1. Ultra-short
  2. Short-term
  3. Long-term
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4
Q

What is another name for ultra-short memory?

A

Sensory memory

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5
Q

What is another name for short-term memory?

A

Working memory

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6
Q

What is an example of ultra-short memory?

A

Echoic memory: someone says something and it lingers for a very short period of time after it’s said

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7
Q

How can we expand the finite limits of our short-term memory?

A

Different behavioral strategies:

  • Episodic buffer
  • Phonological loop
  • Visuospatial sketchpad
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8
Q

How do we make sensory memory into working memory?

A

Attention

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9
Q

What is an episodic buffer?

A

Remember different elements of an experience as an episode

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10
Q

What are the 3 phases of neural activity during working memory?

A
  1. Neural activity during cue presentation
  2. Neural activity during delay period
  3. Neural activity during response
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11
Q

What is a delayed anti-saccade task?

A
  1. Fixation on a point X
  2. Cue presentation in periphery
  3. Cue disappears (delay period)
  4. Response by looking where the cue was presented in periphery
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12
Q

What does the recording of one neuron response to the delayed anti-saccade test show?

A

A neuron responds maximally to a certain part of the visual field = spatial working memory

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13
Q

Where are delay responsive neurons aka short-term memory? What are they responsible for?

A

Dorso-lateral area of prefrontal cortex: area 46 (divided by principal sulcus)

Responsible for keeping track of the position of the flashing cue even while focusing on point X

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14
Q

How do we measure responses to the delayed anti-saccade test in humans? How does it work?

A

fMRI = indirect mechanism to measure neuronal activity

Uses differences between magnetic properties of oxygenated and deoxygenated Hb to measure neuronal activity because we know that firing neurons (aka an active area of brain) need more oxygenated blood

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15
Q

Which is faster: fMRI or recording neuron electrical activity?

A

Recording neuron electrical activity (milliseconds vs seconds)

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16
Q

What is temporal resolution?

A

Speed of test results

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17
Q

What is a BOLD signal?

A

Blood Oxygen Level Dependent signal

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18
Q

What do lesions to the dorsal-lateral prefrontal cortex result in?

A

Impaired spatial working memory

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19
Q

What is delay dependence of the experiments on memory?

A

Important control of experiments because by adding a delay the experiments show deficits have to do with memory because the deficits should get worse as the delay gets longer

If there was no delay the deficit could be due to misunderstanding of the rule, physical problem with response demanded

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20
Q

2 types of long-term memory?

A
  1. Declarative

2. Non-declarative

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21
Q

4 types of non-declarative long-term memory?

A
  1. Non-associative
  2. Priming
  3. Procedural
  4. Conditioning
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22
Q

What is non-associative long-term memory?

A

Discriminating relevant from non-relevant stimuli

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23
Q

2 other names for non-declarative long-term memory?

A
  1. Non-conscious

2. Implicit

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24
Q

2 types of non-associative memory?

A
  1. Habituation

2. Sensitization

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25
Q

What is habituation?

A

Diminished behavior/motor response to a repeated non-noxious stimulus

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26
Q

What is a non-noxious stimulus?

A

Stimulus that is not potentially tissue damaging

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27
Q

Why does habituation not happen when the repeated non-noxious stimulus’ intensity is really high?

A

Habituation is dependent on an ethological survival advantage, so if a stimulus signals danger that could cause damage then habituation is not possible

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28
Q

Describe the precise plasticity occurring during habituation.

A

Decrease of quantity of NT release by the sensory neuron on the postsynaptic motor neuron or interneuron and therefore same effect through the whole pathway

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29
Q

What is the time span of habituation?

A

Can last for weeks

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30
Q

What is sensitization?

A

Administration of a stimulus on another body part results in the progressive amplification of a response to a stimulus on a body part

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31
Q

What were the habituation and sensitization experiments done on?

A

Poking a sea slug’s siphon or tail and measuring the amplitude of the gill withdrawal reflex

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32
Q

What is the time span of sensitization?

A

Less than 3 weeks

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33
Q

What is priming?

A

An implicit memory effect in which exposure to one stimulus influences the response to another stimulus

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34
Q

What are the 3 types of specificities used in priming? Explain each.

A
  1. Stimulus specificity: effects of physical properties of stimulus between study and test (e.g. use same font)
  2. Associative specificity: effects of associations of target items are used between study and test
  3. Response specificity: effects of a change in the required response to a stimulus between the study phase and the test
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35
Q

What is repetition suppression? What can it explain?

A

Memory neural mechanism which attenuates (i.e., gradually decreases the intensity of) signals in the brain when a stimulus is detected repeatedly

Can explain priming

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36
Q

What is procedural memory? What are the 2 characteristics of procedural memory?

A

Skill learning

  1. Requires multiple trials
  2. Subjects do not know what they are learning
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37
Q

What is another name for procedural memory?

A

Implicit memory

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38
Q

What is an important brain structure of procedural memory?

A

Basal ganglia

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39
Q

What is the serial reaction time task?

A

Commonly used parameter for measuring implicit learning.

In a SRT task, participants are asked to repeatedly respond to a fixed set of stimuli in which each cue signals that a particular response (i.e., button press) needs to be made. Unbeknownst to the participant, there are probabilities governing the transition between the cues, and thus required responses following one cue have some predictability. As a result, reaction time (RTs) to these cues becomes increasingly fast as subjects learn and utilize these transition probabilities.

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40
Q

What patients respond poorly to the serial reaction time task?

A

Parkinson’s disease patients

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41
Q

What does a negative mean reaction time difference score mean in the SRT task?

A

Getting faster and faster

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42
Q

Why is the measured outcome of the SRT task mean reaction time difference?

A

You cannot compare raw motor performance between healthy and PD patients, you want to compare whether or not they will improve the speed of their reactions

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43
Q

What is the effect of conscious learning on implicit memory? Why?

A

Learning impairment

Because competition between implicit motor (basal ganglia and cerebellum) and explicit declarative (hippocampus) systems will impair learning!

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44
Q

Describe an experiment that shows the competition between memory systems.

A

Place strategy: swimming towards an exit sign (explicit strategy)
Response strategy: implicit motor function is directing the swimming

  • Micro-injection of glutamate in basal ganglia increases the number of animals that adopt a response strategy
  • Micro-injection of glutamate in hippocampus increases the number of animals that adopt a place strategy
  • Injection of saline first favors the place strategy and after repetition of the exercise favors response strategy
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45
Q

Can injecting glutamate into hippocampus after a response strategy has been developed suppress it?

A

YUP, place strategy will be used instead

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46
Q

In the swim maze example, how can we tell if the animal is using place or response strategy?

A

Move the exit sign and see if the animal starts swimming towards where it was previously (response strategy) or where it is now (place strategy)

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47
Q

What are the 2 types of conditioning? Who discovered each?

A
  1. Classical conditioning (Ian Pavlov)

2. Operant conditioning (BF Skinner)

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48
Q

What is classical conditioning also known as?

A

Pavlovian conditioning

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49
Q

Describe classical conditioning.

A

Stimulus substitution where we pair a neutral stimulus (conditioned stimulus, CS) with a stimulus (unconditioned stimulus, UCS) that evokes a response (unconditioned response, UCR)

Through conditioning, the CS gains the ability to stimulate the response (conditioned response, CR)

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50
Q

What is extinction? Describe it in detail.

A

As the animal learns that the cue or context no longer predicts the coming of the unconditioned stimulus, conditioned responding gradually decreases, or extinguishes.

This is an ACTIVE process

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51
Q

What is the principle of contingency?

A

Refers to how well a conditioned stimulus (CS) predicts your unconditioned stimulus (UCS).

Can be positive or negative:

  • Positive: US is more likely when the CS occurs than when it does not
  • Negative: US is less likely when the CS occurs than when it does not
52
Q

In the Pavlov dog example, if you play the tone only half the time when you give the dog meat, what effect will this have on the conditioning? What does this demonstrate?

A

The rate of conditioning will be slower because the tone (CS) is not a perfect predictor of the food (UCS)

Contingency

53
Q

What is the principle of contiguity?

A

Refers to close temporal proximity (few seconds) needed between the CS and the UCS for conditioning to occur

54
Q

In the Pavlov dog example, if you play a tone (CS) and wait ten minutes before giving the food (UCS) will conditioning occur?

A

NOPE

55
Q

What is the blocking effect? Why does it work this way?

A

Refers to how learning a new conditioned stimulus (CS2) is blocked because a previous conditioned stimulus (CS1) already perfectly predicts the unconditioned stimulus (UCS)

This occurs because CS2 added no new information and does not predict anything new, so therefore the subject doesn’t gain any survival benefit from learning it

56
Q

Is the blocking effect overruled if you increase the intensity of UCS when you add CS2? Why/Why not?

A

YUP because now CS2 adds new information so learning is not blocked

57
Q

What part of the brain does fear conditioning rely on?

A

Amygdala

58
Q

Where is the amygdala?

A

Medial temporal lobe, anterior to hippocampus

59
Q

3 major roles of amygdala?

A
  1. Fear
  2. Reward
  3. Social behavior
60
Q

Describe the fear conditioning process happening in the amygdala.

A
  1. Lateral nucleus receives convergent sensory information from CS and UCS at the critical synapse
  2. Synapse is strengthened by the pairing of CS and UCS
  3. Lateral nucleus neurons project either directly to central nucleus or through basal nucleus and then central nucleus
  4. Central nucleus projects to many parts of the brain to trigger conditioned emotional responses
61
Q

2 input nuclei of amygdala?

A
  1. Lateral nucleus

2. Basal nucleus

62
Q

Output nucleus of amygdala?

A

Central nucleus

63
Q

Where does the central nucleus of the amygdala project to? Role?

A
  1. Hypo
  2. Midbrain
  3. Pons
  4. Medulla

=> will mediate autonomic responses to sensory stimuli the amygdala receives

64
Q

Describe the synapse strengthening that happens in the fear conditioning process happening in the amygdala. What is this called?

A
  • Before conditioning: UCS causes stronger afferent stimulus than CS
  • During conditioning: UCS and CS cause the same afferent stimuli
  • After conditioning: connections between UCS neuron and BLA neuron and between CS neuron and BLA neuron are both strengthened = LTP

= Hebbian plasticity

65
Q

What is operant conditioning?

A

Use of consequences to modify a voluntary, spontaneously emitted behavior (operant)

66
Q

Other name for operant conditioning?

A

Instrumental conditioning

67
Q

Difference between classical and operant conditioning?

A

Classical: response is a reflex
Operant: response is a voluntary behavior

68
Q

How do you modify the frequency of an operant?

A
  1. Punishment: behavior frequency decrease

2. Reinforcement: behavior frequency increase

69
Q

What is Thorndike’s Law of Effect?

A

It states that responses that produce a satisfying effect in a particular situation become more likely to occur again in that situation, and responses that produce a discomforting effect become less likely to occur again in that situation.

70
Q

How did Thorndike come up with his Law of Effect?

A

He put a bunch of hungry cats in a puzzle box with food outside. He found that over progressive trials, the time it took the cats to escape got shorter and shorter. This meant that a desired consequence (getting the food) made the operant behavior (hitting the lever) more likely to occur

71
Q

What are the 2 types of reinforcement? Define them and provide an example.

A
  1. Positive Reinforcement = giving something nice when you perform a behavior (e.g. food pellet for pulling a lever)
  2. Negative Reinforcement = taking away something bad when you perform a behavior (e.g. a constant shock stops every time you touch your lip)
72
Q

What are the 2 types of punishment? Define them and provide an example.

A
  1. Positive Punishment = giving something bad when you perform a behavior (e.g. delivering an
    electric shock every time you pull a lever)
  2. Negative Punishment = taking away something good when you perform a behavior (e.g. taking
    away candy every time you pull a lever)
73
Q

What are the 4 schedules of reinforcement/punishment? Describe each.

A
  1. FR - Fixed ratio: reinforcement should be delivered after a “fixed” number of correct responses
  2. VR - Variable ratio: the delivery of reinforcement will “vary” but must average out at a specific number
  3. FI - Fixed Interval: reinforcement becomes available after a specific period of time.
  4. VI - Variable Interval: the time periods that must pass before reinforcement becomes available will “vary” but must average out at a specific time interval
74
Q

What schedule of reinforcement are slot machines built with?

A

VR

75
Q

List the schedules of reinforcement starting from the one causing the highest number of responses in the shortest amount of time.

A
  1. VR
  2. FR
  3. VI
  4. FI
76
Q

What can inhibit both conditioning and extinction? Why?

A

Protein synthesis inhibitor because we need protein synthesis to learn!

77
Q

What are the 2 types of reinforcers? Describe each.

A
  1. Primary reinforcers = things that animals or people will work for without any experience with them: food, air, water, sleep, sex, and drugs are examples of this (all unconditioned stimuli)
  2. Secondary reinforcers = things that have a conditioned association with one of the primary reinforcers. Money is a good example: we know that money can buy food, so we can be conditioned using money as reinforcement.
78
Q

How are superstitious behaviors acquired?

A

Behaviors picked up during conditioning because subject thinks it somehow affects the outcome (punishment/reward).

79
Q

What can explain phobia development?

A

Fear inducing stimuli could be generalized during conditioning.

80
Q

2 types of declarative memory?

A
  1. Episodic

2. Semantic

81
Q

Define semantic memory.

A

Memory of meanings, facts, and other concept-based knowledge unrelated to specific experiences

82
Q

Define episodic memory.

A

Memory of autobiographical events (times, places, associated emotions, contextual knowledge) that can be explicitly stated

83
Q

Where are semantic memories stored?

A

In the same areas that process the information initially: the color of an object would be stored in visual areas because you see the color. The feel of an object would be stored in somatosensory areas object.

84
Q

What is the role of the temporal pole in semantic memory?

A

Convergence zone for unimodal semantic representations into a multimodal memory

85
Q

Where is the temporal pole?

A

Most anterior portion of the temporal lobe

86
Q

What is a name for multimodal memories? Define it.

A

Gestalt = organized whole that is perceived as more than the sum of its parts

87
Q

What kind of memory is often implicated in amnesia?

A

Episodic memory

88
Q

What are the 2 types of amnesia? Define each.

A
  1. Retrograde = inability to remember events occurring before amnesia onset
  2. Anterograde = inability to form new memories because long-term memory is impaired due to temporal lobe damage
89
Q

Is short-term memory affected in anterograde amnesia?

A

NOPE

90
Q

What disease can cause anterograde amnesia?

A

Herpes simplex encephalitis

91
Q

Is emotional memory affected in anterograde amnesia?

A

NOPE, intact BUT without context

92
Q

What is recognition memory?

A

Form of declarative memory that we can test across species

93
Q

What part of the brain is recognition memory dependent on?

A

Temporal lobe

94
Q

What is temporally graded retrograde amnesia? Why does this occur?

A

Retrograde amnesia where remote memories are more easily accessible than events occurring just prior to the trauma

This happens because our older memories migrate away from our hippocampus and towards our cortex as we consolidate, reactivate, re-experience and restore them.

95
Q

What is Wernicke-Korsakoff syndrome?

A

Due to thiamine deficiency (often because of alcohol abuse), degenerates the mammilary bodies, one of the structures that receives information from the hippocampus as part of the circuit that mediates declarative memory => deficits in declarative memory (explicit)

They also exhibit confabulation, which is basically filling in gaps in their memory with random bits that may not be true.

96
Q

What does damage to the anterior nuclei of the thalamus cause?

A

Deficits in declarative memory (explicit) and confabulation

97
Q

In what patients do we see a shrunken hippocampus? Explain how this happens.

A

Alzheimer’s patients

Damage actually starts with fairly selective damage in the entorhinal cortex. The damage to the entorhinal cortex is consistent with mild cognitive impairment, a prodrome (early hallmark symptom) of Alzheimer’s

98
Q

What do the diseases Alzheimer’s and Wernicke-Korsakoff syndrome illustrate?

A

Brain memory structures do not act in isolation - they are part of circuits

99
Q

What 2 processing streams is declarative memory mediated by? Describe each.

A
  1. Ventral stream: “what” stream = remembers you saw something
  2. Dorsal stream: “where” stream = remembers you saw something in an array in space
100
Q

Where does the declarative memory ventral stream project to?

A

Parietal lobe

101
Q

What brain structure binds the dorsal and ventral streams of declarative memory together? What does this allow for? What is this called?

A

Hippocampus - allows for formation of context rich memories

=> binding-in-context model

102
Q

Describe the pathway of declarative memory.

A

Unimodal and polymodal association areas (frontal, temporal, and parietal lobes) => “What” (ventral) stream comes through the perirhinal
cortex and “Where” (dorsal) stream comes through the parahippocampal/postrhinal cortex => lateral and medial entorhinal cortex => hippocampus, where the two streams are combined to form a sweet new memory with context

103
Q

From where does the parahippocampal cortex receive input?

A

Parietal lobe

104
Q

Describe experimental evidence for the two declarative memory streams and their binding at the hippocampus.

A

Delayed non-match to sample task:

  1. An object is put it in front of the monkey, and the monkey knocks it out of the way and takes the food reward.
  2. You then close a divider between the objects and the monkey, place the same object as well as a new object, and then open the divider
  3. Animals and humans have a preference for novelty so if we have a choice between old and new, we’ll go after the new thing.

If you damage the hippocampus, the monkey will have increasingly severe deficits as you take away more and more of their temporal lobe. They won’t be able to do this task as well. Damage to the perirhinal cortex in particular makes this task harder

105
Q

What kind of damage would impair the normal response to the delayed non-match to sample task? Which has a stronger effect? Why?

A
  1. Damage to hippocampus (via ischemia, aspiration, radio-frequency, excitotoxins…etc)
  2. Damage to perirhinal cortex: stronger effect because this damages the “what” which doesn’t need much context in this exercise (provided by the hippocampus)
106
Q

Is epilepsy surgery done unilaterally or bilaterally? Why?

A

Unilaterally to temporal lobe to avoid amnesia

107
Q

What brain damage inhibits object recog?

A

Perirhinal cortex

108
Q

What brain damage inhibits place recog?

A

Parahippocampal/Postrhinal cortex

109
Q

What brain damage inhibits context recog?

A

Hippocampus

110
Q

What part of the brain is responsible for spatial memory?

A

Hippocampus

111
Q

What experience showed which part of the brain is responsible for spatial memory?

A

In a water maze study you’re essentially dropped in a pool and you have to find your way to a platform that you can’t see. On the walls there are a bunch of things (bright lights, flag, etc..) that help to give you context. The only way that you can learn to do this task better is based on the context clues. Damage to the hippocampus prevents you from learning to do this task better because you can no longer understand the context clues.

112
Q

What is the subiculum?

A

Brain structure that receives input from hippocampus

113
Q

What real-life situation can cause damage to the hippocampus? Symptom?

A

People with transient global ischemia can suffer from damage to the hippocampus because neurons in the hippocampus are very sensitive to O2 deprivation so they tend to die off a lot due to the ischemia.

Individuals with this type of disease have very large deficits in spatial navigation

114
Q

What can happen to memories as they are retrieved/reconsolidated? What do we call this?

A

When you retrieve a memory and are in the process of reconsolidating it, that memory can change => labile memories

115
Q

Where was LTP first discovered?

A

In-vivo rabbit

116
Q

Purpose of LTP?

A

Strong important signals should be remembered and weak ones should be forgotten

117
Q

If you had a glutamatergic synapse with only NMDA receptors, would be able to signal through it? What would we call this synapse?

A

NOPE

Silent synapse

118
Q

What is LTP the basis of?

A

LEARNING

119
Q

What is an inhibitory avoidance task?

A

Positive punishment to decrease frequency of a behavior and increase avoidance of it

120
Q

Difference between repetition suppression and habituation?

A

Habituation is seen on the circuit level

Repetition suppression is seen on the single cell level

121
Q

For extinction, do you necessarily need to use another CS to teach the mouse that it will not get shocked? Or does that just accelerate the extinction process?

A

Simply accelerates the process - not necessary

122
Q

What is acquisition/encoding?

A

The processing of physical sensory input into memory

123
Q

What is consolidation? What is it sensitive to?

A

Process of stabilizing the memory trace

Sensitive to disruption

124
Q

What is retrieval/recall?

A

Act of retrieving from long-term memory a specific incident or fact

125
Q

What is conditioned taste aversion?

A

Example of classical conditioning but takes place over a longer interval of time.

SMP - Neurophysio Exam 2 (9 decks)

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