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Beyond the Dopamine Hypothesis

The Neurochemical Pathology of Schizophrenia

Published online by Cambridge University Press:  02 January 2018

G. P. Reynolds
G. P. Reynolds*
Affiliation:
Department of Pathology, University of Nottingham Medical School, Queen's Medical Centre, Nottingham NG7 2UH
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Abstract

The dopamine hypothesis still provides a valuable approach to the study of schizophrenia and its treatment by drugs. Although the neuroleptic drugs appear to act via an inhibition of dopamine receptors, measurements of dopamine metabolites in vivo, or of the transmitter and its receptors in postmortem brain tissue, do not provide unequivocal evidence of a hyperactivity of dopaminergic neurotransmission in the disease. Nevertheless, increased dopamine function might be a consequence of a primary neuronal abnormality in another system. Recent imaging studies and neuropathological reports suggest that, in some patients, there may be a deficit and/or disturbance of neurons in certain temporal limbic regions, and this is supported by some neurochemical investigations, particularly of neuropeptide and amino-acid transmitter systems. A loss of such neurons could conceivably lead to a disinhibition of limbic dopamine neurons, providing the means whereby neuroleptic drug treatment might ameliorate the effects of a neuronal deficit in schizophrenia.

Type
Review Article
Information
The British Journal of Psychiatry , Volume 155 , Issue 3 , September 1989 , pp. 305 - 316
Copyright
Copyright © Royal College of Psychiatrists, 1989 

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