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Basic Neurophysiology of Antipsychotic Drug Action

  • Chapter
Antipsychotics

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 120))

Abstract

The clinical actions of antipsychotic drugs (APDs) have typically been attributed to their effects on dopaminergic systems in the brain. Despite the controversy regarding whether or not blockade of dopamine (DA) receptors is both necessary and sufficient for APDs to exert their therapeutic actions, it is evident that the mesolimbic and/or mesocortical DA systems play some role in the clinical efficacy of these drugs. Similarly, the development of motor side effects following long-term treatment with classical neuroleptics appears to be contingent on their actions on the motor-related nigrostriatal DA projection. The focus of this chapter will be on reviewing studies of the physiology of DA systems as it relates to APD action, with particular emphasis on DA cell firing, how it is generated, how it is controlled, and how long-term treatment with APDs can lead to its inactivation, a condition known as depolarization block. In addition, this chapter will encompass recently described actions of APDs as they involve the modulation of information processing at a network level within structures receiving dopaminergic input (i.e., the striatum and nucleus accumbens). Briefly, it is now known that the ability of DA to modulate electrical coupling between neurons in these structures can be modified by long-term treatment with APDs. Thus, the actions of APDs within the basal ganglia appear to be rather complex, and several levels of analyses must be synthesized in order to gain a more comprehensive perspective of their actions.

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O‚Donnell, P., Grace, A.A. (1996). Basic Neurophysiology of Antipsychotic Drug Action. 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_6

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