Abstract
Beginning with the finding by Carlsson and Lindqvist (1963) that acute administration of chlorpromazine increases dopamine (DA) turnover, an extensive literature has developed concerning the effects of antipsychotic drug (APD) administration on multiple brain DA systems. Although APDs of different chemical classes can vary markedly in their molecular structure and receptor binding profiles (Hyttel et al. 1985), they all act to some degree as DA receptor antagonists (Seeman et al. 1976; Farde et al. 1988). A wide variety of neuronal mechanisms have been studied in relation to acute and prolonged APD effects on dopaminergic function, including changes in DA receptors, DA receptor-linked second messenger activity, and DA neuron electrophysiology (See and Chapman 1994, for review). Among the many effects of APDs on DA function, the release and turnover of forebrain DA continues to serve as the primary reflection of dynamic APD-induced alterations in neural activity. One aim of the present chapter is to review findings on APD effects on DA release and metabolism.
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See, R.E., Kalivas, P.W. (1996). Tolerance and Sensitization to the Effects of Antipsychotic Drugs on Dopamine Transmission. In: Csernansky, J.G. (eds) Antipsychotics. Handbook of Experimental Pharmacology, vol 120. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-61007-3_7
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