Experimental tardive dyskinesia.

L M Gunne; J E Häggström

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PubMed · 2858481

Experimental tardive dyskinesia.

L M Gunne·J E Häggström

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Abstract

In ongoing studies of chronic administration of neuroleptics to monkeys (Cebus apella) and rats, the regional distribution of glutamic acid decarboxylase (GAD) and brain levels of homovanillic acid were examined. Reduction of GAD activity, a GABA-synthesizing enzyme, in three specific brain areas (substantia nigra, medial globus pallidus, and nucleus subthalamicus) was related to the development of neuroleptic induced dyskinesias; these reductions were not seen in treated animals who did not develop movement disorders. The neostriatal level of HVA was reduced in dyskinetic monkeys. Such animal models can be useful in the screening process for new antipsychotics and thus potentially aid in the prevention of drug-induced tardive dyskinesia.

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Animals Antipsychotic Agents Brain Cebus Corpus Striatum Disease Models, Animal Drug Evaluation, Preclinical Dyskinesia, Drug-Induced Fluphenazine Frontal Lobe Globus Pallidus Glutamate Decarboxylase Haloperidol Homovanillic Acid Rats Substantia Nigra gamma-Aminobutyric Acid Journal Article Research Support, Non-U.S. Gov't

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L M Gunne, J E Häggström. 1985. Experimental tardive dyskinesia.. https://pubmed.ncbi.nlm.nih.gov/2858481/

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