Abstract
Publisher Summary This chapter focuses on the studies of dopamine hypothesis of schizophrenia. The group of disorders known collectively as schizophrenia continues to be a critical problem for modern psychiatry and accounts for large expenditures by society and tragedy for many families. The predominant hypothesis for a neurochemical defect in schizophrenia is the dopamine (DA) hypothesis of schizophrenia, which suggests that there is an excess of DA neuronal activity in specific brain areas in schizophrenic patients. Such excess DA activity could occur through increased presynaptic DA release via increased DA synthesis and/or faulty negative feedback regulation, or through supersensitive postsynaptic DA receptors. The DA hypothesis of schizophrenia is supported by indirect pharmacologic evidence. Drugs such as amphetamine and methylphenidate, which increase central DA function, in high and long-term doses, can produce a paranoid schizophrenic-like syndrome in normal subjects. These drugs also exacerbate positive symptoms, that is, hallucinations, delusions, in schizophrenic patients.
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