The predominant biological hypothesis for a neurochemical defect in schizophrenia is currently the socalled ''dopamine (DA) hypothesis''. In its simplest form, this hypothesis states that schizophrenia may be related to a relative excess of DA dependent neuronal activity. It is derived from pharmacologic evidence that drugs that decrease DA activity (e.g., the phenothiazines) may be antipsychotic and drugs that promote DA activity (e.g., amphetamine) may be psychotomimetic. The particular means by which ''too much dopamine'' is produced in schizophrenia is not yet known. The authors present the more recent evidence for this hypothesis, deemphasizing material covered in previous reviews and including background information on the biochemistry of DA, the function and regulation of DA neurons, the major DA neuronal pathways, and the pharmacology of drugs that affect DA neuronal systems. An understanding of the cell biology, pharmacology, and gross anatomy of DA neurons is essential for a critical evaluation of current evidence regarding the DA hypothesis and for future developments that will probably add additional complexities to the current belief that ''too much dopamine'' may be the neurochemical basis for schizophrenia.
ASJC Scopus subject areas
- Psychiatry and Mental health