Module 2 Flashcards

(40 cards)

1
Q

Dual-process theory of instrumental action

A

Goal-directed (top-down, cognitive control) vs habituation-based (bottom-up, automatic)

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2
Q

Is drug-seeking goal-directed or habitual?

A

Can be both, there is empirical evidence for the view that it is goal-directed, but it can also be habitual

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3
Q

What does goal conflict entail in goal-directed drug seeking?

A

The short-term goal of a rush/suppression of withdrawal can overshadow the long-term goal of health

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4
Q

What is the substantia nigra part of?

A

Basal ganglia

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5
Q

What 2 regions does the SN consist of?

A
  1. SN pars compacta: large number of DA neurons (also in VTA)
  2. SN pars reticulata: more GABA neurons
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6
Q

Parkinson’s disease- SN

A

death of dopamine neurons in SN, movement-related deficits

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7
Q

R-O relationship

A

instrumental response- motivationally relevant outcome (if i do A, i get B), leads to instrumental behavior

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8
Q

By what two criteria is goal-directed action mediated?

A

(cognitive) belief: representation of the R-O relationship
(motivational) desire: representation of incentive value

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9
Q

Habit-based action

A

instrumental behavior that is triggered by contextual stimuli

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10
Q

What does the Law of Effect (Thorndike) say about habit-based action?

A

habits are mediated by S-R links and are therefore autonomous of the desirability

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11
Q

What experimental paradigm is used to determine whether behavior is goal-directed or habitual?

A

outcome-devaluation paradigm

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12
Q

What phases does outcome devaluation consist of in animal research?

A

Instrumental learning-outcome devaluation- critical test

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13
Q

What were the results of outcome devaluation in animal studies?

A

rats are capable of goal-directed action, but overtraining led to a diminished devaluation effect (they kept pressing)

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14
Q

What contributes to vulnerability to maladaptive habits?

A

aberrantly strong habit formation, weak goal-directed control

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15
Q

What kind of behavior is dominant in addiction?

A

S-R habitual control

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16
Q

Results of Tricomi (outcome devaluation) study

A

1-day group showed goal-directed behavior (less for devalued food), 3-day group showed habitual behavior (equal response for both foods)

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17
Q

fMRI results Tricomi

A

posterior putamen/globus pallidus (increased activity) plays central role in habitual behavior
vmPFC (increased activation with increased anticipation, pattern stable): representing the value, supporting goal-directed behavior
S-R association eventually became stronger than vmPFC

18
Q

Main executive functions

A

error monitoring, working memory, cognitive flexibility/set shifting, decision making, inhibitory (impulse) control

19
Q

Neuroimaging studies- executive control deficits related to dysfunction in?

A

PFC, anterior cingulate, orbitofrontal cortex

20
Q

fMRI- addiction conclusions

A
  • gray matter reductions: PFC, cingulate, insula (either consequence or risk factor)
  • white matter: alterations in those that use substances
21
Q

Research paradigms for measuring executive control

A

cognitive flexibility, decision making, inhibitory control

22
Q

Cognitive flexibility measured with? + what is seen in substance abuse?

A
  • WCST: Wisconsin Card Sorting Test
  • perseverative error (failure to change the rule)>lack of cognitive flexibility
23
Q

Decision making tested with? [2] + what is seen in substance abuse?

A

*Delay discounting: subjective value goes down quicker
* IGT: Iowa gambling task (advantageous + disadvantageous decks): participants with mOFC (orbitofrontal cortex) /vmPFC dysfunction + addiction stay on the bad decks

24
Q

Contingency management

A

positive behavioral change is reinforced, long-term goals over immediate gratification

25
How is inhibitory control measured? [3] + what can be seen in people with addiction?
*Go/no-go task: fail to suppress responses to no-go signals *SST: stop-signal task: failure to inhibit the response, especially in harder trials [dACC: dorsal anterior cingulate cortex, less active] * Stroop task: more mistakes + slower responding in incongruent trials
26
Habit theory of substance abuse * researchers * definition
* everitt & robbins * aberrantly strong habits + impaired cognitive control mediate the transition (incorporates dual-process theory)
27
How do goal-directed and habitual behavior tie into habit theory?
* habituation: drugs affect the DA system> habit formation + cravings * goal-directed: PFC affected>weaked goal-directed + cognitive control
28
What is the similarity between incentive-sensitization and habit theory?
they regard behavior as context-dependent
29
Incentive-sensitization theory
* Berridge & Robinson * pathological motivation for drugs + impaired cognitive control lead to addiction
30
Neuroscientific evidence for goal-directed and habitual control (dual-process theory)
parallel pathways * goal-directed: vmPFC, overlaps with OFC and caudate * habit: premotor cortex (PMC) and posterior putamen (in striatum)
31
Do substances have an acute effect on goal-directed action?
Yes, they shift the balance from goal-directed towards habitual control
32
What provides indirect support for the role of habits in addiction?
Self-Report Habit Index (SRHI) + cue reactivity studies (activation striatal habit region)
33
Does drug-seeking become habitual with repetition?
Yes, over time a transition from goal-directed to habit insensitive to devaluation
34
Is habit formation accelerated for drug rewards relative to natural rewards?
yes (more lever pressing for drugs than for food)
35
Does substance abuse lead to a general tendency to fall back on rigid habits?
those with a history of substance abuse tend to rely more on habit-based behavior, so yes
36
Are drug habits compulsive?
habits play a role in the transition from goal-directed towards compulsive drug-seeking (extensive training kept pressing lever)
37
Treatment implications for habit theory
capitalize intact bottom-up processes, strengthen weakened top-down processes
38
What are the [3] major dopamine pathways and to what concept do they add
1. Mesolimbic (VTA-NA): craving (incentive sensitization) 2. Nigtostriatal (SN- posterior putamen): habit formation 3. Mesocortical (VTA-PFC): cognition
39
Pro-arguments for the brain disease model of addiction [3]
1. addiction is a fronto-striatal circuitry disorder (permanent brain changes) [2. neuroimaging as the ultimate diagnostic tool is not realistic: help understand underlying mechanisms] [3. experimental animal models, causal] 4. the brain disease model does not ignore other factors 5. genetic risk is probabilistic, not deterministic 6. total abstinence is relatively rare 7. can help alleviate social stigma
40
Contra-arguments brain disease model [3]
1. some brain functions do show recovery after a period of abstinence 2. brain dysfunction not sufficient for diagnosis 3. neuroimaging studies just offer correlational evidence 4. many other risk factors 5. genetic predisposition does not result in compulsion 6. cases of spontaneous remission 7. other alternatives to the moral model