DOPAMINE HYPOTHESIS AO3

• Support for excess dopamine

  Evidence comes from the fact that amphetamines increase the amount of dopamine. Timmons and Hamilton (1990) report that high doses of amphetamine (a drug that stimulates DA activity) can result in an acute psychosis resembling schizophrenia in clinically normal people.

  Timmons & Hamilton provide support for the excess dopamine hypothesis, as it clearly demonstrates high levels of dopamine being linked with the positive symptoms of schizophrenia which is what the excess dopamine hypothesis predicts.
• Support for dopamine receptor sites

  Gjedde and Wong (1987) who found that schizophrenics have more than twice as many dopamine receptors than controls.

  Gjedde & Wong provide support for the dopamine receptor sites hypothesis in that schizophrenics were found to have twice as many DA receptors, suggesting that the reasons for the high levels of dopamine is due to increased receptor sites.
• Refuting evidence against excessive dopamine

  Davis et al (1991) reported that high levels of dopamine are not found in all schizophrenics, and the modern anti-schizophrenic drug clozapine, with very little dopamine blocking activity, works effectively against the disorder.

  This criticises the dopamine hypothesis suggesting that high levels of DA are not found in all schizophrenics, therefore this cannot be a complete explanation for such a complex disorder. This suggests that there could be other neurotransm
• Refuting evidence against excessive dopamine

  The Excessive dopamine explanation does not explain whether the excess dopamine activity was responsible for the positive symptoms, negative symptoms, or both. Drugs did not work for individuals who had negative symptoms.

  One issue with the excess DA hypothesis is that it cannot explain whether this neurotransmitter is responsible for the positive symptoms, negative symptoms or both...therefore cannot be a complete explanation for schizophrenia. There could be other biological factors that are not explained by the dopamine explanation.
• Methodological issue with the dopamine hypothesis

  Direct measurements of neurotransmitter levels like dopamine is flawed. Neurotransmitter levels are measured by the metabolite levels in patients’ cerebrospinal fluid.

  One methodological issue of the DA hypothesis is that levels of DA are measured through a lumbar puncture – this is a painful procedure and levels of neurotransmitters can be impacted by diet etc. Until we have refined procedures for measuring neurotransmitter, be cautious in the conclusion we draw from metabolite-based research.
• Reductionist - dopamine hypothesis 


  The dopamine hypothesis can also be accused of being over-simplistic, as any other neurotransmitters may also be involved in the development of schizophrenia.

  It is reductionist because it ignores the role of social factors which could contribute to the development of schizophrenia.

  Epidemiologists (people who work in a branch of science that examines the prevalence of diseases) claim that a series of factors increase the risk of developing schizophrenia, including being migrant, being male, living in an urban environment, and being born poor.
• Deterministic - dopamine hypothesis


  Weakness - biologically deterministic. This is because if the individual does have excessive amounts of dopamine then does it really mean that they will develop schizophrenia? The dopamine hypothesis ignores individual differences. Linked with this idea is the suggestion that dopamine seems to be associated more with positive symptoms, so it may contribute only to certain aspects of the disorder. Alternatively, this could also suggest that there are several types of schizophrenia, with dopamine linked to certain types only.
• schizophrenia summarised


  It is clear that schizophrenia is a complex disorder and that there are many neurotransmitter systems involved in the production of the various symptoms. It is unlikely that any one hypothesis will be shown to be the dominant one.
• conclude dopamine hypothesis AO3

  What seems to be emerging is that the dopamine system is critically involved in some of the positive symptomology, serotonin is likely to be involved in some of the negative symptomology, and that glutamate is probably important in terms of the effect that disruption to this system has on the dopamine system. However, how these systems fully interact is the subject of current research and we can only speculate at this stage as to the interactions between the three systems.