Task 7: Adding affect Flashcards

1
Q

A1: Revise the location of the amygdala

A

Aymgdala (AMY)

  • diencephalon
  • medial temporal lobe
  • part of limbic system
  • end of hippocampus (HC)
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2
Q

A1: Why is the AMY relevant for goal-directed decision making & neuroeconomics?

A

Neuroeconomics assumed rationality, but people show non-rational behaviour/heuristics-based choices/biases/…

  • E.g. framing, emotional impact of winning or losing
  • > AMY is crucial in this
  • > also “tags” events/objects/actions with affective value (positive & negative) -> influences stimulus-action-outcome associations made by the cortex
De Martino (2006)
- AMY activation is related to risk-aversion & risk-seeking -> framing effect
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3
Q

A1: What are the two major misconceptions about AMY function?
1) negative or positive?
+ Monkey evidence

A

1) AMY is only involved in negative emotions, as “protection device”
- Fear conditioning is commonly used to model emotional learning
- But evidence for positive processing too

Monkey evidence
Paton (2006):
- single-neuron measurement in monkeys conditioned to associate visual stimuli with positive/negative valence which was swapped after some time
- If AMY only represents negative -> activity should change
- Results: Activity for both reward & punishment, activity just reversed
-> single cells in AMY respond to stimuli valence independent of positive/negative valence
-> AMY activity reflects stimulus-valence learning & later reflect switching

Braesicke:

  • viewing high-/low-incentive food, anticipatory (AP) vs. consummatory periods (CP)
  • before lesion: skeletomotor responses in AP & cardiovascular in both AP & CP
  • after AMY lesion: no cardiovascular response in AP & still other 2 responses
  • > AMY contributed to positive affective association with conditioned stimulus

Study on reinforcer devaluation

  • no lesion -> sensory-specific satiety, food preference available
  • AMY lesion -> no sensory-specific satiety, intact preference
  • > AMY role is limited to updating monkey’s estimation of current value of food
  • > once updated AMY is not needed for choice (representations of expected food value stored elsewhere)
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4
Q
A1: What are the two major misconceptions about AMY function?
1) negative or positive?
\+ Rat evidence
\+ Human evidence
\+ conclusions
A

Rats learn S-R associations -> later spend more time near associated stimulus

  • > tendency to associate physically with positive stimuli
  • Central AMY nucleus lesion -> no approach behaviour
  • BLA lesion -> no approach behaviour
  • > both regions of AMY mediate positive affect

Somerville

  • humans learning face + name + valence associations
  • right AMY
  • > selectively sensitive to emotional descriptions (both positive & negative)
  • > generates nonspecific arousal signal
  • > could also encode stimulus-valence associations

Johnsrude

  • subjects preferred images paired with high-reward probability (vs. low/mid)
  • AMY lesion -> no more preferences
  • > AMY mediates an association between sensory inputs & their affective valence
  • > People can be unaware of the associations but behaviour is the basis of them
  • > Role of AMY is just as important for positive emotions as for negative ones
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5
Q

A1: What are the two major misconceptions about AMY function?

2) S-R?
- Reasoning
- Monkey evidence

A

2) AMY contributes to S-R learning & emotions are by-product of reinforcement
Rationale:
- AMY lesion -> impaired reward-based object selection
-> interpreted as: AMY forms S-R & by-product emotions
-> BUT: inaccurate lesions

Monkey studies for emotional reaction (without S-R)

  • Task: grab food from box with spider or neutral object
  • Healthy -> intact emotional reaction (hesitating + defensive reaction to spider vs. neutral)
  • AMY lesion -> no hesitation or defensive reaction

Evidence against involvement of reward processing

  • precise AMY lesion -> no impaired “object-reversal learning” and “win-stay lose-shift” task
  • > both are S-R tasks that do not depend on AMY
  • > lesion had no effect on S-R but on emotional responses -> need to be differentiated
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6
Q

A2: Specify the role of AMY in goal-directed decision making
Keyword: AMY-OFC network (Murray)

A

AMY has reciprocal connections with OFC & sensory areas (IT, PRh)

AMY -> OFC interaction: affective info

1) AMY updates reward values
- > only temporarily necessary for acquiring S-R
2) OFC stores reward values
- > always necessary
- AMY lesion -> OFC can’t store S-R properly
- OFC -> AMY: feedback, important for updating
- Decision-making is guided by these outcome values

IT/PRh -> OFC interaction: processing visual info

  • implementing visually guided rules (e.g. object reversal learning)
  • AMY not involved in object-reversal learning tasks

AMY -> IT/PRh interaction: attentional modulation
- enhanced sensory processing of significant stimuli/events

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7
Q

A3: Briefly explain the following terms:

  • Rationality
  • Framing effect
  • Loss aversion
A

Rational decision-making: Invariance/consistency in choices regardless of how choices are presented

Framing effect: Same information given different meaning based on its framing

  • possible explanation: incomplete information -> relying on heuristics
  • Gain frame -> risk-aversion -> chose sure over gamble option
  • Loss frame -> risk-seeking -> chose gamble over sure option
  • > subjects are unaware, frame does not affect RTs

Loss aversion: Tendency to prefer avoiding losses to acquiring equivalent gains

e. g. of 50€ you lose 30€ or get 20€
- > stronger meaning given to loss than to win

Risk-aversion vs. loss-aversion

  • LA -> deals with difference between gain vs. loss frame without choice for gambling
  • RA -> deals with difference between safe vs. gamble choices within gain frame
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8
Q

A3: Describe De Martino’s neuroeconomics experiment

  • AMY
  • MCC
A

fMRI:

  • Choices in line with framing effect (G(sure) + L(gamble))
  • > increased activity in bilateral AMY
  • > decreased activity in MCC (+ even SMA)
  • Choices opposite to framing effect/more rational (G(gamble) + L(sure))
  • > decreased activity in bilateral AMY
  • > increased activation in MCC (+ even SMA)
  • -> AMY activation is related to risk-aversion & risk-seeking in line with framing effect
  • independent of valence
  • framing effect is driven by heuristics by emotional system
  • -> MCC (+ even SMA) activation suggests opponency between 2 systems
  • MCC -> detecting conflicts between “analytic response tendencies” (rational choices)
  • AMY -> detecting more “emotional” tendencies (heuristic choices)
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9
Q

A3: Describe De Martino’s neuroeconomics experiment

- OMPFC

A

OMPFC activity correlated negatively with subjects’ susceptibility to framing effects

  • not predicted by AMY activity
  • strong reciprocal connections between AMY & OMPFC (Murray)

Current theory:

  • OMPFC incorporates inputs from AMY
  • OMPFC represents value of stimuli -> to guide future behaviour

More rational individuals:

  • may have better representations of own emotional biases
  • > ability to modify behaviour appropriately (e.g. when biases are suboptimal)
  • -> evidence for a model in which OMPFC evaluates/integrates emotional & cognitive information
  • -> this underlies more “rational” behaviour + ability to notice own heuristics + susceptibility to framing effect
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10
Q

A3: Discuss how De Martino’s study confirms Murray’s hypothesized role for AMY

A

Reminder:
Murray:
- AMY updates outcome values -> OFC then stores outcome values

De Martino:

  • AMY active for heuristic decisions
  • OMPFC active for susceptibility to framing effects

Current theory!:

  • OMPFC incorporates inputs from AMY
  • > evidence for a model of OMPFC evaluating/integrating emotional & cognitive information -> leading to more rational behaviour
  • > Murray describes exactly such a model
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11
Q

A4: Explain the Hampton (2007) experiment on reward expectancy & rule switching

  • Aim
  • Methods
A

Aim:

  • AMY & OFC/vmPFC activate to rewarding/punishing outcomes & subsequent behavioural decisions
  • Hypothesis: AMY lesion -> OFC/vmPFC deficit in neural representations of reward expectancy

Methods:

  • 2 patients with focal bilateral AMY lesion, SM & AP vs. 41 matched healthy controls
  • Reversal learning task
  • > learn choice-reward association
  • > flexibly switch choices when rule is changed
  • > probabilistic (p(reward)<1) vs. deterministic (p=1) task variety
  • analysed switch trials vs. stay trials
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12
Q

A4: Explain the Hampton (2007) experiment on reward expectancy & rule switching

  • Results in healthy participants
  • Behavioural choice signal
A

Switch trials: greater activation in

  • anterior frontal insula
  • > reflects increased cognitive control in response to negative feedback prior to response scheme switch (in the next trial)
  • posterior lateral OFC (PLOFC)
  • > S-R storage + updating
  • > negative feedback (prior to switch trials) on previously rewarded stimuli is important update trigger!!
  • MCC
  • > monitoring outcome + response error

Stay trials: decreased activity in

  • mPFC
  • > less cognitively demanding
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13
Q

A4: Explain the Hampton (2007) experiment on reward expectancy & rule switching:

  • Results in healthy participants
  • Expected Reward Signal
A
  • significant correlation with signal in mOFC & mPFC
  • > time-locked
  • > increased linear with increasing expected reward value
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14
Q

A4: Explain the Hampton (2007) experiment on reward expectancy & rule switching:

  • Results in healthy participants
  • Responses to reward/punishment
A
  • Reward -> significant activation in mPFC & mOFC

- Punishment -> significant activation in anterior lPFC & lOFC

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15
Q

A4: How do Hampton’s results fit with the two previous tasks (cortex reward & error monitoring) & Camille (2011)
- Insula, vmPFC, lPFC, lOFC, MCC

A

Insula

  • Task 6 -> error + negative feedback
  • Here -> error + negative feedback leading to switch

vmPFC
Task 5 -> Default network
Here -> less cognitive energy needed

lPFC

  • Task 5 -> state representation
  • Here -> specific activation to punishment

lOFC

  • Task 5 -> Value representation (S-R) + updating (e.g. for satiety)
  • Here -> S-R storage + updating due to error + negative feedback (expected reward, rule-switching)

MCC

  • Task 5 -> action selection, outcome evaluation (A-O)
  • Task 6 -> error detection
  • Here -> error detection, leading to rule-switching

Camille (2011)

  • similar reversal learning task
  • > OFC damage -> more errors during initial learning/fewer reversal -> for stimulus value
  • > MCC damage -> more errors during initial learning -> for action value
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16
Q

A5: Explain the Hampton (2007) experiment on reward expectancy & rule switching

  • Results in AMY lesion participants
  • Behavioural choice signal
A

Switch trials: lower activity in

  • anterior frontal insula
  • posterior lateral OFC
  • MCC
  • > AMY signal doesn’t reach these areas -> less updating
  • > AMY influences these areas & thus influences behavioural choice
17
Q

A5: Explain the Hampton (2007) experiment on reward expectancy & rule switching

  • Results in AMY lesion participants
  • Expected Reward Signal
A
  • no linearly increasing activity for increased expected reward signals in mPFC
18
Q

A5: Explain the Hampton (2007) experiment on reward expectancy & rule switching

  • Results in AMY lesion participants
  • Responses to reward/punishment
A
  • no difference between patients & control

- > Processing rewarding & punishing feedback in OFC & mPFC seems to remain intact after AMY lesion

19
Q

A5: Explain the Hampton (2007) experiment on reward expectancy & rule switching
- Summary

A

AMY lesions selectively impair generating expected reward signals + signals of behavioural choice (which normally are based on those expected rewards) but AMY lesions don’t affect generation of reward outcome signals

20
Q

A5: Present the apparent contradiction between Murray’s claims about the AMY & Hampton’s results

A

Apparent contradiction

  • Murray: AMY doesn’t play a role in S-R learning
  • > not essential for reversal learning (Monkey-Spider-Box) -> lesion only affects emotional response not S-R
  • Hampton: AMY does play a role in S-R learning
  • > lesion lead to decreased reversal learning

BUT -> AMY can be involved but not essential for S-R learning

21
Q

A5: Explain how the results in Hampton actually confirm Murray’s theory about the amygdala

A

Hypothesis: Outcome information consists of affective & reward value

  • AMY signals affective value
  • DA neurons signal reward value
  • > both send signal to lOFC/vmPFC/aMCC/(Pre)SMA

Unexpected reward -> positive emotions -> affective “tag” given to reward -> signalled via feedback -> updating of valence of an event

  • Healthy -> 2 sources of valence info (reward + affective)
  • AMY lesion -> only 1 source of valence info (only reward)

Murray: reward value system is sufficient for S-R associations
Hamptom: AMY influences S-R task performance via affective tagging
- damage -> still possible but worse performance

–> Hampton’s results do support the notion that the reward system alone is sufficient for performing S-R reversal tasks BUT the amygdala adds information that improves performance

22
Q

A6: How does Murray’s AMY-OFC network model match Rushworth’s model?

A

Murray -> then Rushworth:

1a) AMY -> OFC (S-R formed, affective value)
1b) IT/PRh -> OFC (visual processing)

2) lOFC (S-R, value assignment)
3) vmPFC/mOFC (S-R, comparison/object selection)
4) MCC (A-O, action selection)

-> stimulus-reward forming -> stimulus-reward storing -> stimulus-reward comparing -> using stimulus-reward choice for action selection