Task 6 Flashcards

1
Q

6.1: What’s part of the anterior cingulate cortex (ACC)?

A
  • pregenual ACC –> social processing
  • subgenual ACC–> in mPFC; reward-related processing
  • -> often loosely defined
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2
Q

6.1: Which function does the ACC generally have?

A
  • “a”ffective cortex of CC

- value based -affective & self-centred

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3
Q

6.1: What’s part of the medial cingulate cortex (MCC)?

A
  • posterior (pMCC)

- anterior (aMCC)

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4
Q

6.1: Which function does the MCC generally have?

A
  • “m”otor part of CC

- motor related, based on previous action outcome monitoring

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5
Q

6.1: What’s the last division that makes up the CC next to ACC & MCC?

A

posterior CC (PCC)

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6
Q

6.1: What is CC’s relation to the superior frontal gyrus (SFG)?

A
  • SFG= larger section that includes (pre)-SMA

- -> above aMCC

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7
Q

6.2: What’s the functional role of the (a)MCC in goal-directed decision making?

A
  • error detection after comparing intended & actual movement
  • encodes relationship between an action & the outcome (reward & error)
    ==> encodes whether an action is worth performing based on the value of the expected outcome
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8
Q

6.2: What’s the role of the SFG in goal-directed decision making?

A
  • implicated in task control & action selection when set of rules is changed or when action rules must be selected
  • involved in ERN
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9
Q

6.2: What’s the proposed functional division between the anterior/inferior MCC and posterior/superior part (SFG/pre-SMA actually)?

A
  • aMCC: error detection & encoding of action-outcome associations
  • pre-SMA (Rushworth: SFG): response conflict monitoring & selection of action-selection rules when actions are changed or initiated
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10
Q

6.2: What’s a parallel of this dual organization with the similar dual organization of the object
selection regions, as discussed in task 5?

A

-separate structures for storing/updating outcome
information & for using it to come to a current decision
–> Object selection:
-aMCC (action-outcome associations) similar to -> lOFC: keeps track of changing values of objects
– pMCC –> vmPFC: concrete decisions

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11
Q

6.2: What’s the link with task 1 & what was said there about voluntary action selection?

A

o SFG/pre-SMA: uses stored action-outcome associations to decide about the best action in ongoing situation ==> ACTION SELECTION

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12
Q

6.3: Camille et al’s experiment –> rationale; research question

A
  • neural substrates of action value have yet to be definitively established
  • separate structures for stimulus-value vs. action-value learning?
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13
Q

6.3: Camille et al’s experiment –> basic findings

A
  • -> OFC damage:
  • sig. more errors while learning initial associations & completed sig. fewer trails in stimulus-value task
  • sig. more likely to shift away/strategy after win in stimulus value task
  • -> MCC damage:
  • sig. more errors while learning initial action-value associations
  • sig. more likely to shift away after win in action-value task
  • -> no sign. differences after losses
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14
Q

6.3: Camille et al’s experiment –> conclusion of role of OFC & MCC

A
  • OFC: role in value-based choices between stimuli

- MCC: role in value-based choices between actions

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15
Q

6.4: fMRI experiment by Ullsperger et al. (2003) -previous research on MCC

A
  • MCC: involved in ERN

- as a result of habenular inhibition

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16
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - hypotheses

A
  1. Larger activity in habenular on errors with negative feedback vs lower activity on correct responses with positive feedback
  2. Selective increase in MCC activity for negative feedback on errors
17
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - methods

A
o DAMP task-observing two balls
o Watch it role across screen 
o Had to say which ball seems faster 
o Task difficulty was adapted
--> Wanted to keep difficulty constant (how often person was correct/incorrect) 
--> creates response conflict
18
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - results –> when was ventral striatum activated?

A

Ventral striatum (nucleus accumbens) was activated only when positive feedback occurred (correct answer trial) –> probably due to phasic DOPA release

19
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - results –> when was habenular complex (HC) active?

A
  • HC: more highly activated during negative feedback (in error answer trial) than all other conditions
  • HC: more highly activated in correct trials without feedback, than error trials without feedback (bc of uncertainty)
20
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - results –> pattern of HC activity on error trials (without vs with feedback)

A
  • Without= higher uncertainty –> you don’t expect error –> higher inhibition of HC (lower activation in HC)
  • With= lower uncertainty –> you expect punishment –> lower inhibition of HC (higher activity in HC)
21
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - which structure does HC inhibit?

A
  • midbrain nuclei (VTA & substantia nigra pars compacta)
  • -> inhibits DOPA release
  • -> disinhibits MCC
22
Q

6.4: fMRI experiment by Ullsperger et al. (2003) - when does MCC show its highest activity?

A

MCC specifically reacts on errors followed by informative (negative) feedback

23
Q
  1. 5: Describe ERN (=error-related negativity)

- -> what does it reflect?

A
  • peaking between 50-130 ms after error response
24
Q

6.5: What’s the presumed source of the ERN?

A

MCC

25
Q

6.5: ERN - links with Ullsperger et al (2003) model –> when & why did ERN occur in his experiment?

A

-ERN results from disinhibited neuronal activity in MCC attributable to phasic depression of the dopaminergic activity on errors

26
Q

6.4: When & why is MCC (dis)inhibited in Ullsperger et al’s study (2003)?

A
  • MCC specifically reacts on errors followed by informative (negative) feedback
  • dopa activation –> MCC inhibited
  • HC active –> inhibits midbrain nuclei –> phasic depression of dopa –> MCC disinhibited –> SO MCC active
27
Q
  1. 5: ERN - links with Rushworth et al (2004) (correct model)
    - -> role of MCC
    - -> role of pre-SMA
A
  • MCC: detects when actions have led to errors
  • error detection is just one aspect of a more general MCC role in associating actions with their outcomes even when these are positive rewards
  • -> pre-SMA: monitoring of response conflict before error commission
28
Q

6.6: ERN & error-monitoring + psychopathology –> distinction activity in ACC & MCC

A
  • ACC –> emotional/affective activity

- MCC –> cognitive activity

29
Q

6.6: ERN & error-monitoring –> OCD

A
  • hyperactive error-processing
  • larger ERNs
  • magnitude of ERN correlated to OCD symptoms
  • higher ACC resting activity
30
Q

6.6: ERN & error-monitoring –> Depression

A
  • hyperactive error processing
  • increased ERN
  • increased feedback negativity signal (negative dip shortly after feedback; indicates worse than expected outcome)
31
Q

6.6: ERN & error-monitoring –> Schizophrenia

A
  • HYPOactive error processing
  • decreased ERN
  • ACC: smaller BOLD signal to go/no-go task
  • negative symptoms: motivational deficits, loss of speech, catatonia, reduced performance monitoring
  • -> inverse correlation betw. negative symptoms & ERN magnitude
32
Q

6.4: pre-SMA in Ullsperger model

A

errors led to higher activity regardless of feedback compared to being correct

33
Q

6.4: Ullsperger model –> MCC

A

most active when making error when getting feedback

34
Q

6.4: Ullsperger model –> habenular complex

A
  • error –> no feedback ==> less active
  • error –> feedback ==> very active
  • correct –>no feedback –> very active (bc of uncertainty)
  • correct –> feedback –> less active
35
Q

Which brain area does DOPA usally inhibit?

A

DOPA inhibits MCC activity

36
Q

What is conflict theory & is it correct?

A

ERN related to response conflict; not dissociated ==> INCORRECT! THEY ARE ACTUALLY DISSOCIATED!