Carlsson

• Aim:

  1. explore rival theory, that of glutamatergic deficiency & hypoglutamatergia.
  2. present current view of relationship between SZ & dopaminergic dysfuntion.
• Procedure

  Literature Review (33 total, 14 he was involved).

  'Beyond dopamine' --> drugs like PCP reduce glutamate & ketamine produces psychotic symptoms.

  PET scans: yellow/red = active.
• Results (1): Dopamine hypothesis

  high dopamine in schizophrenia, especially basal ganglia.

  Laruelle says SZ in remission have normal dopamine levels:

  Explains why patients in remission on antipsychotics complain of side effects --> no shock as drugs cause hypodopaminergia.
• Results (2): glutamate hypothesis

  Lodge: glutamate activity at NMDA receptors produce psychotic symptoms in rats & humans.

  PCP & ketamine = psychotic symptoms, instead activating glutamate receptors and not dopamine.
• Results (3): Glutamate & Dopamine

  Glutamate regulates behaviours of dopamine activity.

  Miller & Abercrombie: release of dopamine increases if glutamate receptors are blocked (decrease).
• Conclusion

  SZ subpopulation --> some dopamine hypothesis & others glutamate deficiency.

  Advises researchers to look into other neurotransmitters such as gaba & acetylcholine
• Generalisability

  high.

  33 total, 14 he's in.
• Reliability

  (-) Laruelle not published so not peer-reviewed.

  (+) standardisation of lab setting & PET.
• Application

  developed antipsychotics & improved dopaminergic drugs.
• Validity

  (-) temporal validity --> 1999.

  (+)objective data (PET).
• Ethics

  (-)Deception (some SZ given placebo drug).

  (+)No human harm (majority animals)