Should atypical antipsychotics be able to modulate rather than impair PFC dopaminergic transmission?
Beyond ‘neuronal and dopaminergic’ dopamine We have recently shown that the dopaminergic output in the rat PFC could be an expression of the activity of noradrenergic neurons as well.92 Atypical antipsychotics by blocking DA autoreceptors localized on noradrenergic neurons would increase DA and NE output not only from DA neurons but from noradrenergic neurons where these two monoamines may act as cotransmitters. In the same area approximately 35% of the total D2 ligand binding activity is known to be associated with astrocytes isolated from rodents (mice and rats) and primates (monkeys and humans), while astrocytes isolated from D2 receptor knock-out mice failed to show any D2-ligand binding.93 The functional nature of these receptors is sustained¾directly¾by the fact that a 25% increase in intracellular Ca2+ is induced after the local application of the D2-receptor-specific agonist quinpirole, an effect reversibly blocked by the substituted benzamide raclopride; and¾indirectly¾by the
