Abstract
Rats treated with haloperidol that developed vacuous chewing movements (VCM), a possible animal model of tardive dyskinesia, were studied with quantitative autoradiography for dopamine type-1 (D1) and type-2 (D2) receptors as well as dopamine re-uptake sites. Haloperidol increased striatal D2 receptors, but did not affect D1 receptors or the dopamine re-uptake site. D2 receptor increases occurred in rats with and without VCMs. In so far as VCM is a model for tardive dyskinesia, haloperidol induced increases in striatal D2 receptors do not appear to be etiologic for these abnormal movements.
MeSH terms
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Animals
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Autoradiography / methods
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Benzazepines / metabolism
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Biological Transport
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Corpus Striatum / metabolism*
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Dopamine / metabolism*
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Dopamine D2 Receptor Antagonists
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Dyskinesia, Drug-Induced / metabolism*
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Ligands
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Male
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Mastication
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Piperazines / metabolism
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Raclopride
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Rats
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Rats, Sprague-Dawley
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Receptors, Dopamine D1 / metabolism*
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Receptors, Dopamine D2 / metabolism*
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Salicylamides / metabolism
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Tritium
Substances
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Benzazepines
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Dopamine D2 Receptor Antagonists
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Ligands
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Piperazines
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Receptors, Dopamine D1
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Receptors, Dopamine D2
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Salicylamides
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Tritium
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Raclopride
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1-(2 (diphenylmethoxy)ethyl)-4-(3-phenylpropyl)piperazine
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Dopamine