evaluating dopamine

• SUPPORTING SCIENTIFIC RE

  Volkow et al (03) fMRI - during drug intoxication > areas associated with dopamine - activated

  including b circuits involved with reward, motivation and cognitive control

  shows link between dop and substance A > credible explanation
• CONTRADICTORY EVIDENCE > doesn't explain all types

  Stokes et al (09) - no significant increase in dop for volunteers who took cannabis (depressant)

  Yoder - no consistent increase in dop across people who took alc (depressant)

  engage in AB > doesn't produce an increase in dopamine } insufficient explanation - explains some not all > is gene explanation better

  Counter = Professor Nutt (15) - criticised method

  sample - often small and ppts given substances in different form and in a lab
• USEFUL APPLICATIONS FOR TREATMENT - therapy - target strategies to reduce rewarding dopamine properties

  E.G. Naltrexone - antagonist for AB

  binds to opioid receptors and blocks AB effects > if used = no pleasure / increase in dopamine > Ab - less rewarding and less likely to engage

  prevents dop release by binding and blocking

  gives validity to theory that dop release is involved in A

  antagonists - most effective when used with other methods - suggests dopamine isn't the sole cause
• REDUCTIONIST

  A - complex B > reduced to role of dopamine and reward pathways

  AB - very complex > explanation = too simplistic and ignores other important influences with supporting research evidence (Bosari and Carey)
• CONCLUSIONS

  explanation is valid : scientific, supporting evidence, successful applications and dop can be scientifically tracked and measured

  lacks reliable and conclusive evidence, unlikely to be sole cause, reductionist