Initially dopamine hypothesis suggested that an excess (too much) of the neurotransmitter dopamine in certain regions of the brain is associated with positive symptoms of SZ
SZ are thought to have abnormally high numbers of dopamine receptors on receiving neurons, resulting in more dopamine binding and more neurons firing
Dopamine hypothesis - evidence
Drugs that increase dopamine levels - amphetamines and L dopa both increase dopamine levels and are linked to SZ symptoms
Drugs that decrease dopamine levels - all antipsychotic drugs block dopamine levels and decrease hallucinations
The revised dopaminehypothesis - positive
Proposed that positive symptoms of SZ are caused by an excess of dopamine in subcortical areas of the brain, especially the mesolimbic pathway
The revised dopamine hypothesis - negative
The negative and cognitive symptoms arise from a deficit of dopamine in areas of the prefrontal cortex (mesocortical pathway)
Evidence for revised hypothesis
Neural imaging - PET scans show lower levels of dopamine in prefrontal cortex of SZ
Animal studies - Study reduced dopamine levels in prefrontal cortex in rats, resulting in cognitive impairments. This was then reversed using an atypical antipsychotic