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Chronic neuroleptic treatment: D2 dopamine receptor supersensitivity and striatal glutamatergic transmission
Author(s) -
Calabresi Paolo,
De Murtas Marco,
Mercuri Nicola Biagio,
Bernardi Giorgio
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410310404
Subject(s) - haloperidol , glutamatergic , dopamine , postsynaptic potential , excitatory postsynaptic potential , glutamate receptor , dopamine receptor d2 , neurotransmission , dopamine receptor , chemistry , neuroscience , cholinergic , neurotransmitter , medicine , pharmacology , endocrinology , receptor , biology
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.