Pavlovian conditioning and association Flashcards

1
Q

What is learning?

A

Lecture 1, slide 9

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2
Q

What experiment did Cross et al conduct in 1967? What was its hypothesis, purpose and results?

A

Lecture 1, slide 10-11, 14-15

-the rats showed preference for Mozart over Schoenberg

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3
Q

What is the difference between Pavlovian learning (classical conditioning) and Instrumental learning?

A
  • Pavlovian learning: learning about the relationship between different stimulus events
  • Instrumental learning: learning about the relationship between an organisms own responses and stimuli
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4
Q

What did Pavlov’s experiments show? What are the two explanations for a conditioned response?

A

Lecture 1, slide 24, 27

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5
Q

How can we measure learning with behaviour?

A

Lecture 1, slide 29-30

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6
Q

Give three examples of excitatory conditioning.

A

Lecture 1, slide 31

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7
Q

What is extinction and spontaneous recovery?

A

Lecture 1, slide 36-37

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8
Q

What effect does changing the intensity/salience of the US have on learning/behaviour?

A

Lecture 1, slide 38-40

-increasing intensity/salience: stronger and quicker learning

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9
Q

What is congruency in learning? Give an example of a study that shows that some stimuli are resistant to association.

A

Lecture 1, slide 44

-some associations are harder to learn than others

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10
Q

Describe the Pavlovian eye-blink conditioning in humans.

A

Lecture 1, slide 46

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11
Q

What is habituation and what is sensitisation? What animal is used to model them and why?

A

Lecture 1, slide 47-48

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12
Q

What is filled traced conditioning? What is an occasion setter?

A

Lecture 1, slide 50

-stonger learning in filled trace conditioning (experimental) than trace conditioning (control)

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13
Q

What is higher-order learning? What is sensory preconditioning?

A

Lecture 1, slide 51-52, 54

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14
Q

What is conditioned inhibition? How can we test whether a CS has been inhibited?

A

Lecture 1, slide 55-59

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15
Q

What are the temporal constraint for eliciting a CR?

A

Lecture 1, slide 28

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16
Q

How does the probability and rate of US presentation affect learning?

A

Lecture 2, slide 3

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17
Q

How does contingency affect learning? What evidence is there for this effect?

A

Lecture 2, slide 5-8

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18
Q

What is a conditioned stimulus? What is a conditioned response?

A

Lecture 2, slide 10

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19
Q

What study did Siegel carry out in 1982? What was the method and what were the results

A

Lecture 2, slide 11-16

-context seems to be a/the CS

20
Q

What is patterning?

A

Lecture 2, slide 17-18

21
Q

What are the different theories of hippocampal function? What aspects of relational learning may the hippocampus be required for?

A

Lecture 2, slide 25, 27

22
Q

What was the lesion study and results of the study conducted by Iordanova in 2011? Can episodic memories be explained by associative learning?

A

Lecture 2, slide 28-31
-can episodic memories be explained by associative learning: maybe not, because in this study, hippocampal lesions don’t destroy the rats’ ability to learn associations, but seems to be important for configuring more complex episodes.

23
Q

What is Pavlovian conditioning used to study?

A

Lecture 2, slide 33

24
Q

Explain the gradual learning curve?

A

Lecture 2, slide 34

25
Q

Is learning gradual or a result of insight?

A

Lecture 2, slide 35-43

26
Q

What is Hull’s computational theory of error correction in learning? How can it be used to explain acquisition and extinction?

A

Lecture 2, slide 44-50

27
Q

What is overshadowing?

A

Lecture 2, slide 51

-more salient cue interferes with the learning of weaker cues

28
Q

What is Kamin’s blocking effect?

A

Lecture 2, slide 52

-prior learning of CS1 interferes with learning of CS2

29
Q

What is the Rescorla-Wagner theory? What learning effects/phenomena does it explain that Hull’s theory cannot?

A

Lecture 2, slide 53-64

30
Q

What is relative value and its importance?

A

Lecture 2, slide 65

31
Q

What study did Wagner conduct in 1968? What is relative validity?

A

Lecture 3, slide 3-11

  • in the True Discrimination group, CS2 and CS3 are more valid than CS1. They reliably signal occurance and nonoccurance of US.
  • in the PseudoDiscrimination group all 3 cues are equally valid (50% chance of US)
  • if one cue is mor valid it interferes with the learning of another cue
32
Q

What is over expectation?

A

Lecture 3, slide 11-12

33
Q

What is super conditioning? What is protection from extinction?

A

Lecture 3, slide 14-20

34
Q

How is Schizophrenia related to prediction error correction and selective learning?

A

Lecture 3, slide 21, 27

35
Q

What study was conducted by Serra et al in 2001?

A

Lecture 3, slide 28-29

36
Q

What effect does increasing the strength of the US have on blocking? What was the study carried out by Dickinson et al (1976)? What are positive and negative prediction errors?

A

Lecture 3, slide 32-33

-if the strength of the US is unexpected then there will be learning

37
Q

What is latent inhibition?

A

Lecture 3, slide 34

38
Q

What role does dopamine have in learning? What type of DA responses can you have in learning? What is reward substitution?

A

Lecture 3, slide 41-44

39
Q

What study was conducted by Waelti et al in 2001?

A

Lecture 3, slide 45-47
-RPE: reward error prediction
In their study, Kamin blocking was used to generate prediction errors. Monkeys were trained to know visual stimuli A and B (control) were followed by juice (reward) and not followed by a reward respectively. This conditioning was followed up with compound training where BY+ triggered more behaviour from the monkey than B- (which triggered no behaviour after conditioning) whereas AX+ triggered the same amount of as behaviour as A+. DA neurons of the VTA showed more activity when the monkey was presented with BY+ than just B-, but activity remained similar for both AX+ and X+. X- minus has been blocked by A+ and so it cannot be learnt about. This is a failure to form new cue-reward associations due to the lack of RPE signal. The monkey has already been conditioned to expect a reward when presented with A+, so the presentation of a reward with AX+ does not deviate from what is expected and nothing is learnt from the experience. On the other hand, the presentation of BY+ was not predicted by either stimulus and therefore receiving a reward should have generated a positive prediction error.

40
Q

What study was conducted by Tobler et al in 2003?

A

Lecture 3, slide 48-49

-X is learnt to be inhibitory

41
Q

What is the difference between latent inhibition, overshadowing and blocking?

A

classical conditioning is undermined by preexposure to the CS (latent inhibition) or the concurrent presentation of either a more salient CS (overshadowing) or one that has already been associated with the US (blocking).

  • latent inhibition: preexposure to CS prevents learning/acquisition of a CR
  • blocking: CS1 has already been associated with the US. This blocks learning of CS2
  • overshadowing: CSa is more salient than CSb. Concurrent presentation of CSa and CSb, reduces learning of the less salient CSb.
42
Q

What are some causal manipulations to determine the function of a structure?

A

Lecture 4, slide 2

43
Q

What are optogenetics? What are the steps to optogenetics?

A

Lecture 4, slide 4

44
Q

What study was carried out by Steinberg et al., 2013?

A

Lecture 4, slide 6-7
-RPE: reward error prediction
-they utilised optogentics to demonstrate that DA released by dopaminergic cells of the VTA behave as positive RPE signals.
-In the first stage of the experiment two groups of rats (a blocking group and a control group) were conditioned with a single cue—tones A and B respectively. This was followed by compound testing where AX (tone and light) was presented to both groups followed by a sucrose drink (reward). A test was subsequently performed to determine how much the rats had learnt about the light stimulus (X). As expected, the blocking group had not learnt much about the light due to blocking and the lack of a RPE, while the control group were able to learn about the light. The differences in learning were significantly different at a 99.9% confidence level since p=o.oo3.
-The aim of the next stage of the experiment was to determine whether increasing the DA firing rate of VTA dopaminergic cells at the point of US administration would be sufficient to unblock the learning of light in the blocking group. There are three groups involved in this method: PairedCre+, UnpairedCre+ and PairedCre-. The Cre- group consists of wildtyepe rats. The two Cre+ groups consitst of transgenic rats which express Cre recombinase under the control of the tryosine hydoxylase promoter. All of three groups received identical injections of a Cre-dependent virus expressing channelrhodopsin-2 into their VTA. The Cre- individuals did not take up the channelrhodopsin due to their lack of Cre, whereas the channelrhodopsin’s were inserted into the VTA dopaminergic neural membranes of the Cre+ groups, enabling their DA neurons to increase their activity in the presence of light.
All 3 groups were trained in a way that normally causes blocked learning. However, during the compound training, the two paired groups received the light/optical stimulation paired with the US, while the unpaired group received the stimulation during the inter-trial interval.
The results of this experiment succeeded in showing that VTA DA is involved in learning through acting as a RPE signal. The PairedCre+ group showed learning of the light cue unlike the other two groups. Typically due to blocking and the lack of an unexpected stimuli, the DA neurons would not fire, however the artificial firing of DA in response to light mimics the naturally occurring prediction error signal, allowing the rats to learn.

45
Q

What are the limitations of the studies that have proposed dopamine as a learning signal?

A

Lecture 4, slide 8