The dopamine hypothesis is a long standing explanation for psychosis and schizophrenia. The theory developed aside the abundance of research into dopamine during the 1960’s and 1970’s which was encouraged by dopamine being recognized as an important neurotransmitter in the brain (Carlsson , Lindqvist, Magnusson, & Waldeck, 1958). It suggests that schizophrenia is the result of an imbalance of the neurotransmitter dopamine, which is related to the brains reward and pleasure pathways. Individuals with schizophrenia have been found to have abnormally high numbers of D² receptors on their neurone synapses leading to increased neurone firing and thus higher levels of dopamine. Van Rossum (1966) suggested the theory of schizophrenia and psychosis is the result of over active dopamine pathways in the brain. His research provided evidence that neuroleptic drugs block dopamine receptors in the central nervous system indicating that these drugs are successful due to their ability to reduce levels of dopamine (Van Rossum, 1966).
Supporting research includes antipsychotic drugs, such as thorazine and haldol, which reduce psychotic symptoms by blocking dopamine activity in the brain. (gleitman, Gross & Reisberg, 2011).Van Rossum and Hurkmans (1964) showed that the psychomotor stimulating effects of dexamphetamine and cocaine were due to direct and/or indirect stimulation of dopamine receptors suggesting a link between psychotic behaviour and dopamine. Temporary psychosis has been induced in mentally sound individuals when over dosing on high amounts of amphetamines (of which stimulate dopamine activity) (gleitman, Gross & Reisberg, 2011). Also, evidence derives from individuals with Parkinsons disease as many are found to have low levels of dopamine. Individuals that were given the drug L-dopa, that increases dopamine levels, were found to develop symptoms similar to that of schizophrenia (Grilly, 2002).
However, more current research suggests that the symptoms of schizophrenia are more likely to be influenced by both deficits and excesses of dopamine in the brain rather than merely over active dopamine production (Abi-Dargham, 2004). The updated dopamine hypothesis indicates that there is a co-existing deficit of dopamine in the cortex and an excess in the sub cortex of individuals with schizophrenia (Abi-Dargham, 2004). The revised theory is still not conclusive as other neurotransmitters have also been found to produce schizophrenic type symptoms such as glutamate. The blockage of glutamate receptors by the illegal drug Phencyclidine induces schizophrenic-like symptoms (Gorelick & Balster, 1995). Also, the increase in glutamate levels has been found to alleviate positive and negative symptoms of schizophrenia (Goff & Coyle, 2001).
Therefore this suggests that the dopamine hypothesis is too basic to explain schizophrenia and rather a theory that incorporates the effect of a variety of neurotransmitters and/or their pathways is more plausible.
Abi-Dargham, A. (2004). Do we still believe in the dopamine hypothesis? New data bring new evidence. International Journal of Neuropsychopharmacology, 7(1), 1-5. doi: 10.1017/S1461145704004110
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Gleitman, H., Gross, J., Reisberg, D. (2011). Psychopathology. In Snavley, S. L. (8. Ed.) Psychology Eighth Edition (pp 664-666). New York, London: Norton & Company, Inc.
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