Historically the beneficial effects of classical antipsychotic agents were explained by their action on brain pathways in which dopamine is the neurotransmitter. Dopaminergic pathways include the tuberoinfunibular pathway (moderating prolactin release from the hypothalamus), the nigrostriatal pathway (involved in motor control and deficient in Parkinson's Disease) and the mesolimbic pathway, which runs from the ventrotegmental area via the nucleus accumbens to the prefrontal cortex (Fig. 19.3) (and is overactive in psychotic illness according to the dopamine hypothesis of schizophrenia). Five dopamine receptor types are identified. Dj- and D5-receptor activation increases intracellular cyclic AMP concentrations whereas activation of D„ D3 and D4 subtypes has the opposite effect. Since all classical antipsychotic agents shared an ability substantially to block D2-receptors, their effects in ameliorating psychosis were ascribed to preventing activation of these receptors. Thus it was postulated that the key deficit in schizophrenia was increased dopaminergic activity, brought about by a rise in the number of brain dopamine D2-receptors, or receptor supersensitivity, or excess availability of dopamine for D2-receptor activation from overproduction or reduced destruction through enzyme deficiency.
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