Task 6 Flashcards
6.1: What’s part of the anterior cingulate cortex (ACC)?
- pregenual ACC –> social processing
- subgenual ACC–> in mPFC; reward-related processing
- -> often loosely defined
6.1: Which function does the ACC generally have?
- “a”ffective cortex of CC
- value based -affective & self-centred
6.1: What’s part of the medial cingulate cortex (MCC)?
- posterior (pMCC)
- anterior (aMCC)
6.1: Which function does the MCC generally have?
- “m”otor part of CC
- motor related, based on previous action outcome monitoring
6.1: What’s the last division that makes up the CC next to ACC & MCC?
posterior CC (PCC)
6.1: What is CC’s relation to the superior frontal gyrus (SFG)?
- SFG= larger section that includes (pre)-SMA
- -> above aMCC
6.2: What’s the functional role of the (a)MCC in goal-directed decision making?
- 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
6.2: What’s the role of the SFG in goal-directed decision making?
- implicated in task control & action selection when set of rules is changed or when action rules must be selected
- involved in ERN
6.2: What’s the proposed functional division between the anterior/inferior MCC and posterior/superior part (SFG/pre-SMA actually)?
- 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
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?
-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
6.2: What’s the link with task 1 & what was said there about voluntary action selection?
o SFG/pre-SMA: uses stored action-outcome associations to decide about the best action in ongoing situation ==> ACTION SELECTION
6.3: Camille et al’s experiment –> rationale; research question
- neural substrates of action value have yet to be definitively established
- separate structures for stimulus-value vs. action-value learning?
6.3: Camille et al’s experiment –> basic findings
- -> 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
6.3: Camille et al’s experiment –> conclusion of role of OFC & MCC
- OFC: role in value-based choices between stimuli
- MCC: role in value-based choices between actions
6.4: fMRI experiment by Ullsperger et al. (2003) -previous research on MCC
- MCC: involved in ERN
- as a result of habenular inhibition
6.4: fMRI experiment by Ullsperger et al. (2003) - hypotheses
- Larger activity in habenular on errors with negative feedback vs lower activity on correct responses with positive feedback
- Selective increase in MCC activity for negative feedback on errors
6.4: fMRI experiment by Ullsperger et al. (2003) - methods
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
6.4: fMRI experiment by Ullsperger et al. (2003) - results –> when was ventral striatum activated?
Ventral striatum (nucleus accumbens) was activated only when positive feedback occurred (correct answer trial) –> probably due to phasic DOPA release
6.4: fMRI experiment by Ullsperger et al. (2003) - results –> when was habenular complex (HC) active?
- 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)
6.4: fMRI experiment by Ullsperger et al. (2003) - results –> pattern of HC activity on error trials (without vs with feedback)
- 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)
6.4: fMRI experiment by Ullsperger et al. (2003) - which structure does HC inhibit?
- midbrain nuclei (VTA & substantia nigra pars compacta)
- -> inhibits DOPA release
- -> disinhibits MCC
6.4: fMRI experiment by Ullsperger et al. (2003) - when does MCC show its highest activity?
MCC specifically reacts on errors followed by informative (negative) feedback
- 5: Describe ERN (=error-related negativity)
- -> what does it reflect?
- peaking between 50-130 ms after error response
6.5: What’s the presumed source of the ERN?
MCC
6.5: ERN - links with Ullsperger et al (2003) model –> when & why did ERN occur in his experiment?
-ERN results from disinhibited neuronal activity in MCC attributable to phasic depression of the dopaminergic activity on errors
6.4: When & why is MCC (dis)inhibited in Ullsperger et al’s study (2003)?
- 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
- 5: ERN - links with Rushworth et al (2004) (correct model)
- -> role of MCC
- -> role of pre-SMA
- 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
6.6: ERN & error-monitoring + psychopathology –> distinction activity in ACC & MCC
- ACC –> emotional/affective activity
- MCC –> cognitive activity
6.6: ERN & error-monitoring –> OCD
- hyperactive error-processing
- larger ERNs
- magnitude of ERN correlated to OCD symptoms
- higher ACC resting activity
6.6: ERN & error-monitoring –> Depression
- hyperactive error processing
- increased ERN
- increased feedback negativity signal (negative dip shortly after feedback; indicates worse than expected outcome)
6.6: ERN & error-monitoring –> Schizophrenia
- 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
6.4: pre-SMA in Ullsperger model
errors led to higher activity regardless of feedback compared to being correct
6.4: Ullsperger model –> MCC
most active when making error when getting feedback
6.4: Ullsperger model –> habenular complex
- error –> no feedback ==> less active
- error –> feedback ==> very active
- correct –>no feedback –> very active (bc of uncertainty)
- correct –> feedback –> less active
Which brain area does DOPA usally inhibit?
DOPA inhibits MCC activity
What is conflict theory & is it correct?
ERN related to response conflict; not dissociated ==> INCORRECT! THEY ARE ACTUALLY DISSOCIATED!
