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

✍ Scribed by Dr Paolo Calabresi; Marco De Murtas; Nicola Biagio Mercuri; Giorgio Bernardi

Publisher
John Wiley and Sons
Year
1992
Tongue
English
Weight
807 KB
Volume
31
Category
Article
ISSN
0364-5134

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✦ Synopsis

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.

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Clozapine and molindone administered to mice for 21 days did not elevate the density of striatal 3H-spiperone binding sites at doses clinically equivalent to 1.5 mg/kg haloperidol, which elevated binding by 29%. Thioridazine (25 mg/kg) elevated binding by 25%. It appears that clinically equivalent d