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• The dopamine hypothesis explains schizophrenia as a result of abnormal activity of the neurotransmitter dopamine.
• drugs that reduce schizophrenia symptoms are dopamine receptor antagonists: They reduce dopamine activity. The implication is that schizophrenia is caused by increased dopamine activity and that these drugs work by reducing dopamine activity.
• • Dopamine agonists: Several studies have demonstrated that drugs that increase dopamine activity – dopamine agonists, such as amphetamines – can induce schizophrenic symptoms in non-schizophrenic people. For example, a systematic review by Curran et al (2004) found that amphetamine use makes schizophrenia symptoms worse in schizophrenic patients.
• • Further, McKetin et al (2013) found that non-schizophrenic methamphetamine addicts demonstrated a 5-fold increase in schizophrenia-like symptoms during periods when they were using methamphetamine. This link is further supported by animal studies, such as Randrup and Munkvad (1966), who were able to induce schizophrenic behaviour in rats with amphetamines and then reverse these symptoms with dopamine-reducing drugs (antagonists).
• • Post-mortem evidence: Bird et al (1979) used post-mortems to compare dopamine levels in the brains of 50 schizophrenic patients with 50 non-schizophrenic controls. The schizophrenic patients had increased dopamine concentrations in some areas of the brain compared to controls.
• • Brain scans: Some studies using brain-scanning techniques have found increased dopamine activity in schizophrenic patients. For example, Lindström et al (1999) compared PET scans of 12 schizophrenic patients with 10 controls and found the schizophrenic patients had increased dopamine activity in the striatum and parts of medial prefrontal cortex. Further, a review of MRI scans by Alves et al (2008) found support for the (revised) dopamine hypothesis.
• research suggests that schizophrenia is linked with high dopamine activity in some areas of the brain (e.g. the subcortex) but low dopamine activity in other areas (e.g. prefrontal cortex).
• One strength of the dopamine hypothesis is the strong empirical support from neuroimaging and pharmacological studies. For example, research using PET scans has shown that individuals with schizophrenia have higher dopamine activity in key brain areas such as the striatum (Howes et al., 2012). Additionally, the effectiveness of antipsychotic drugs, which work by blocking dopamine receptors, provides further evidence. Typical antipsychotics like chlorpromazine reduce positive symptoms by inhibiting dopamine transmission, suggesting that dopamine overactivity plays a causal role.
• However, this explanation is limited as not all patients respond to dopamine-based treatments, indicating that other neurotransmitters, such as glutamate, may also be involved. This suggests that while dopamine dysregulation is significant, it is unlikely to be the sole explanation for schizophrenia.
• A further limitation of the dopamine hypothesis is that it is largely correlational and does not establish causation. It remains unclear whether excess dopamine causes schizophrenia or whether having schizophrenia leads to changes in dopamine levels. Longitudinal research is needed to clarify whether dopamine abnormalities precede the onset of symptoms.
• • Conflicting evidence: Farde et al (1990) compared brain scans of 18 schizophrenia patients with 20 non-schizophrenic controls. They found no difference in dopamine activity between the two groups. Similarly, in a review of post-mortem studies, Haracz (1982) found little evidence to support the dopamine hypothesis.
• Psychiatrist David Healy (2002) argues that pharmaceutical companies exaggerated the dopamine hypothesis of schizophrenia to sell more drugs. The overly-simplified hypothesis that schizophrenia is caused by high dopamine makes it easy to market antipsychotic drugs as ‘cures’ for schizophrenia.
• : Evidence suggests that other neurotransmitters besides dopamine are involved in the development of schizophrenia, such as glutamate and serotonin. For example, a meta-analysis of brain scans by Marsman et al (2013) found decreased glutamate activity in schizophrenic patients compared to controls. Further, like with the dopamine hypothesis, there is some evidence that drugs that alter glutamate activity can successfully treat schizophrenia.
• • Dopamine is a neurotransmitter. It is one of the chemicals in the brain which causes neurons to fire. The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages.
•  High dopamine activity leads to acute episodes, and positive symptoms which include: delusions, hallucinations, confused thinking.

  • Evidence for this comes from that fact that amphetamines increase the amounts of dopamine . Large doses of amphetamine given to people with no history of psychological disorders produce behavior which is very similar to paranoid schizophrenia.
•  The dopamine hypothesis suggests that schizophrenia is due to dysfunctional dopamine neurotransmission either due to hyperdopaminergia in the subcortex (overly high levels of dopamine) linked to positive symptoms or hypodopaminergia in the cortex (low levels of dopamine) linked to negative symptoms.
• • This original version of the DH posits the idea that hyperdopaminergia (‘hyper’ = more)  in the sub-cortex (sub = beneath) may be responsible for the onset of schizophrenia
• Hyperdopaminergia assumes that an excess of dopamine is active in these central areas, the effect being an altered perception of the world e.g. positive symptoms such as auditory hallucinations 
• • The newer version of the DH posits the idea that hypodopaminergia (‘hypo’ = less)  in the prefrontal cortex (PFC) may be responsible for the onset of schizophrenia
  • The PFC of the brain is thought to control and regulate
  • Hypodopaminergia assumes that low levels of dopamine in the PFC are linked to negative symptoms such as speech poverty: as the PFC plays a  role in logical thinking, low levels of dopamine may lead to the inability to construct grammatical sentences
• • Current understanding of the role of dopamine in schizophrenia is that both hyperdopaminergia and hypodopaminergia may be at work in different brain areas to produce schizophrenia