Abstract
An alteration in the function of dopamine (DA) has been related to the pathophysiology of schizophrenic illness and has led to the so-called “dopamine hypothesis of schizophrenia.” Although there has been only indirect evidence to support this hypothesis (see Meltzer and Stahl, 1976), this has stimulated extensive clinical research for investigating the role of DA in schizophrenic illness. The initial research was directed either toward studying the levels of DA and its metabolites in urine, plasma, and CSF or examining the enzymes associated with the biosynthesis and metabolism of DA in schizophrenic patients. In particular, these studies attempted to elucidate the role of presynaptic dopaminergic mechanisms in schizophrenia. However, in recent years the role of postsynaptic mechanisms such as DA receptor response or DA receptor density has been studied in patients with schizophrenic illness. Such studies have been primarily stimulated by the observations that the potency of antipsychotic drugs is related to their ability to block DA receptors in the brain.
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