Dopamine

Question 1

DOPAMINE (DA)

Answer 1

• neurotransmitter (chemical released by neurons to transmit electrical signa between 2 neurons)
• produced by dopaminergic neurons in ventral tegmental area (VTA)/substantia nigra (SN) in midbrain
• several dif receptor types (D1-D5):
  1) D1 = more abundant in PFC
  2) D2 = more abundant in striatum

Question 2

DOPAMINE PATHWAYS

Answer 2

• dopaminergic signalling occurs via several dif pathways:
  1) mesolimbic pathway
  2) mesocortical pathway
  3) nigrostriatal pathway
  4) tuberoinfundibular pathway

Question 3

DOPAMINE x ADDICTION

Answer 3

• modern DA theories emphasise learning/motivation > pleasure (aka. hedonic impact of rewards)
• drugs of abuse enhance DA function by acting on midbrain neurons to transiently increase extracellular DA concentrations
• prediction errors play key role in addiction development
  SCHULTZ (1998)
• DA neurons encode reward prediction error aka. discrepancy between expected/gained reward

Question 4

BROZOSKI (1979)

Answer 4

• dopamine depletion in monkey PFC causes deficit in spatial WM nearly as severe as complete ablation aka. removal

Question 5

PARKINSON’S DISEASE (PD)

Answer 5

• PD = gradual loss of dopamine neurons in nigrostriatal pathway
• 1980/90s studies found deficits in executive control (ie. planning/WM/attentional set-shifting)
• primarily motor disorder aka:
  1) bradykinesia (slow movement)
  2) akinesia (impairment of voluntary movement)
  3) tremors
• currently no cure BUT treatments include:
  1) L-dopa (dopamine precursor)
  2) recently developed deep brain stimulation

Question 6

COOLS ET AL. (2007): PROCEDURE

Answer 6

• impaired task-set shifting in PD patients
• pps required to either name letter/number on each trial depending on background screen colour:
  1) crosstalk condition
• both numbers/letters presented together; pps had to focus on relevant stimuli /ignore irrelevant
  2) no-crosstalk condition
• number/letter presented alone

Question 7

COOLS ET AL. (2007): RESULTS

Answer 7

• PD patients = significantly impaired relative to healthy controls on switch trials (when required to switch between naming letters & numbers) BUT only in crosstalk condition
• PD patients = deficit in task-set shifting esp. under conditions of attentional distraction

Question 8

EXECUTIVE CONTROL

Answer 8

• 1 theory suggests that dopamine might play dif roles depending on action site:
  1) D1 (^ in PFC) = function linked to stability of representations
  2) D2 (^ in striatum) = function linked to flexible beh
• dopamine might achieve stability/flexibility balance by exerting dif effects on striatal/PFC activation

Question 9

DODDS ET AL. (2008): PROCEDURE

Answer 9

• examined effects of methylphenidate (used to treat ADHD) on brain activation during reversal learning
• methylphenidate = DA reputake inhibitor aka. prevents re-absorption post synapse release -> overall increase in extra-cellular DA lvls
• gave healthy pps probabilistic reversal learning task in MRI scanner
• pps presented w/2 abstract visual patterns in each trial; must discover which 2 patterns are correct via trial-n-error feedback
• feedback = presented upon choice
• contingencies switch post several correct trials aka. pps must also switch to other pattern

Question 10

DODDS ET AL. (2008): RESULTS

Answer 10

• examined in which brain areas activation was modulated by methylphenidate when pps switched response from 1 pattern to another; only region showing such modulation = putamen (part of striatum)
• aka. results show key hole for striatal dopamine in mediating cognitive flexibility

Question 11

DUAL ROLE

Answer 11

• evidence consistent w/dual role for DP in maintaining stability of responding (PFC)/enabling flexible switching (striatum)
• maybe dopaminergic signalling in striatum accounts for individual differences in traits (ie. impulsivity) aka. risk factors for neuropsychiatric disorders (ie. ADHD)

Question 12

COOLS ET AL. (2007): PROCEDURE

Answer 12

• examined effects of bromocriptine (D2 receptor antagonist) on switching beh/neural activation in striatum
• fixation cross colour instructed pps to encode faces/scenes
• trials were either:
  1) switch (attend to dif stimulus than previous)
  2) nonswitch (attend to same stimulus as previous)

Question 13

VAN SCHOUWENBERG ET AL. (2010)

Answer 13

• models of basal ganglia (striatum) acting as “gate” allowing/preventing new goal states into PFC
• current goal states (tasks/stimulus-response contingencies) = represented by coalitions of neurons in PFC
• representations remain stable while pp = focused on current task/goal
• BUT when reward contingencies change/new info becomes available (requiring responding switch) -> DA signalling in basal ganglia prevents responding to previously relevant stimuli allowing establishment of new PFC representation
• aka. enables dif stimulus to gain response control

Question 14

SUMMARY

Answer 14

• OFC plays key role in executive function
• PD involves deficit in cognitive flexibility suggesting role for striatal DA
• effects of DA on executive function may depend on action site:
  1) striatum = cognitive flexibility
  2) PFC = cognitive stability