Chronic neuroleptic treatment: D2 dopamine receptor supersensitivity and striatal glutamatergic transmission

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Abstract
We studied the in vitro electrical activity of rat neostriatal neurons following chronic neuroleptic treatment. In haloperidol‐treated rats, unlike naive animals, activation of neostriatal D2 dopamine receptors induced a potent presynaptic inhibition of glutamate‐mediated excitatory synaptic potentials. Haloperidol treatment did not affect the intrinsic membrane properties of the neostriatal neurons. Pre‐ and postsynaptic physiological responses to direct and indirect gamma‐aminobutyric acid (GABA)–ergic and cholinergic agonists were not affected by chronic haloperidol treatment. These findings suggest that movement disorders induced by chronic neuroleptic treatment may result, at least in part, from a hypersensitivity of presynaptic D2 dopamine receptors regulating the release of glutamate.