Neural correlates:

• The original dopamine hypothesis

  Based on the discovery that drugs used to treat schizophrenia (antipsychotics, which reduce dopamine) caused symptoms similar to those in people with Parkinson's disease, a condition associated with low DA levels Seeman

  • Therefore schizo might be the result of high levels of DA (hyperdopaminergia) in subcortical areas of the brain
  • IE: an excess of DA receptors in pathways from the subcortex to Broca's area (responsible for speech production) may explain specific symptoms of schizophrenia such as poverty of speech and/or auditory hallucinations
• Updated versions of the dopamine hypothesis

  Davis et al proposed the addition of cortical hypodopaminergia i.e. abnormally low DA in the brain's cortex

  • Explain symptoms of schizophrenia

  IE: low DA in the prefrontal cortex (responsible for thinking) could explain cognitive problems i.e. negative symptoms of schizophrenia

  • It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia - so both high and low levels of dopamine in different brain regions are part of the updated version
• Updated versions of the dopamine hypothesis:

  As well as explaining the links between abnormal DA levels and symptoms, current versions of the dopamine hypothesis try to explain the origins of abnormal DA function.

  So it seems that both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical hypodopaminergia and hence subcortical hyperdopaminergia (Howes et al)