Tiagabine inhibits haloperidol-induced oral dyskinesias in rats
| Autor: | X. M. Gao, T. Kakigi, M. B. Friedman, Carol A. Tamminga |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Agonist
Male Dyskinesia Drug-Induced Tiagabine medicine.drug_class Drug Evaluation Preclinical Nipecotic Acids Pharmacology Tardive dyskinesia Placebo Rats Sprague-Dawley otorhinolaryngologic diseases Haloperidol Medicine Animals Single-Blind Method Biological Psychiatry gamma-Aminobutyric Acid business.industry medicine.disease Rats Psychiatry and Mental health Disease Models Animal Neurology Dyskinesia Mastication Neurology (clinical) medicine.symptom business Reuptake inhibitor medicine.drug Progabide |
| Zdroj: | Journal of neural transmission. General section. 95(1) |
| Popis: | Chronic administration of haloperidol to male Sprague Dawley rats for 6 months at a dosage of 1.5 mg/kg/day produces oral dyskinesias in a significant percent of the treated group. This has been used as an animal model of tardive dyskinesia in several laboratories, because the rat movements display characteristics reminiscent of the human dyskinetic condition. Previously, we have reported a reduction in these haloperidol-induced oral dyskinesias with the coadministration of a direct acting GABA agonist progabide. Here, we have tested an indirect acting GABA agonist, tiagabine, coadministered with haloperidol, for its effect on the oral dyskinesias. At a dosage of 75 mg/kg/day tiagabine significantly inhibited the onset of vacuous chewing movements (VCMs), decreasing the average movement severity from 11.2 +/- 2.0 to 4.4 +/- 1.4, compared with a placebo rate of 1.3 +/- 0.5 (VCMs/5 min). These data support the proposition that an effective, potent GABAmimetic coadministered with haloperidol, will block the onset of rat oral dyskinesias. This conclusion has important implications for the treatment and prevention of tardive dyskinesia in humans. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|