The Dopamine Hypothesis
The dopamine hypothesis suggests that excess dopamine in the brain possibly causes schizophrenia. There is an increase of activity at dopamine synapses, which is associated with increased feelings of paranoia. It also explains why hallucinations may occur, as the brain is too active. Over stimulation of the mesolimbic pathway is thought to be linked to positive symptoms of schizophrenia, whilst problems with dopamine functioning in the mesocortical pathways is associated with negative symptoms.
The dopamine hypothesis has been supported by evidence consistently showing a positive correlation between schizophrenia and dopamine. Seeman (2006). In fact, paranoia is drug users where dopamine levels are kept too high, such as amphetamines and cocaine, also supports the role of dopamine in the positive symptoms of schizophrenia.
The effectiveness of drugs that reduce availability of dopamine, leading to a reduction is positive symptoms, supports its role in the disorder. However, although antipsychotic drugs reduce dopamine availability in a very short time the effect on symptoms takes several weeks to appear, suggesting other factors are involved. Additionally, PET scans in those who have had the disorder for many years show blocking of dopamine receptors by antipsychotic drugs does not match a reduction in symptoms, questioning the role of dopamine. Finally, as excess dopamine is only measured after onset of schizophrenia, it could may be an effect, not a cause, of the disorder.