Gamma-acetylenic GABA in tardive dyskinesia

Casey, Dympna; Gerlach, J; Magelund, G.

doi:10.1016/0361-9230(79)90198-9

Cited by 10 publications

(13 citation statements)

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“…Several biological mechanisms of TD have been hypothesized, including dopamine receptor supersensitivity [5] , dysfunction of the serotonergic system [6] and ␥ -aminobutyric acid insufficiency [7] . However, the pathophysiological mechanisms of TD are not well understood.…”

Section: Introductionmentioning

confidence: 99%

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

Na¹,

Choi²,

Paik³

et al. 2007

Neuropsychobiology

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Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotics. We evaluated whether a candidate functional polymorphism of the dopamine D4 receptor (DRD4) gene is associated with drug-induced TD in 209 Korean schizophrenic patients with TD (n = 83) and without TD (n = 126) who were matched for antipsychotic drug exposure and other relevant variables. There was no significant association of the genotype and allele frequencies determined by the –521 C/T SNP of DRD4 between TD and non-TD patients. In addition, there was no significant difference in terms of total Abnormal Involuntary Movement Scale scores among the 3 genotype groups. Within the limitations imposed by the size of the clinical sample, these findings suggest that the DRD4 –521 C/T SNP does not contribute significantly to the risk for TD.

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Section: Introductionmentioning

confidence: 99%

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

Na¹,

Choi²,

Paik³

et al. 2007

Neuropsychobiology

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“…GABAmimetic compounds have already been reported to have an acute therapeutic effect on dyskinetic symptoms in humans with TD (Tamminga etal., 1979(Tamminga etal., , 1983Casey et al, 1980) and on VCMs in rats (Gunne etal., 1982;Mithani et al, 1987). Based on both clinical and experimental data, it appears that regional differences in GABA activity may be responsible for tardive dyskinesia in humans and VCMs in rats.…”

Section: Discussionmentioning

confidence: 98%

Tiagabine inhibits haloperidol-induced oral dyskinesias in rats

Gao

Kakigi

Friedman

et al. 1994

J. Neural Transmission

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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.

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“…In the human clinical studies with THIP (Korsgaard et al 1982;Thaker et al 1987), GAG (Casey et al 1980), and GVG (Korsgaard et al 1983;Stahl et al 1985;Thaker et al 1987) the patients received the test drugs orally for some weeks in doses much lower than in the present experiment. The patients also, as a rule, received concomitant neuroleptic medication.…”

Section: I)ise~onmentioning

confidence: 99%

“…In laboratory animals, GAG has been shown to increase brain and CSF GABA levels several-fold, decrease DA turnover, and partially block DA agonist-induced behavioral effects (Palfreyman et al 1978;Ferkany et al 1979;Lrscher et al 1979). In a controlled clinical study with GVG there was a significant decrease in TD scores with doses up to 225 mg/day (Casey et al 1980).…”

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confidence: 99%

GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

Andersson

Häggström

1988

Psychopharmacology

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Tetrahydroisoxazolopyridinol (THIP), a GABA receptor agonist, gamma-acetylenic-GABA(GAG) and gamma-vinyl-GABA(GVG), two GABA transaminase inhibitors were given in single parenteral doses to three Cebus apella monkeys with persistent dyskinetic movements induced by earlier long-term administration of haloperidol. High doses of THIP temporarily abolished dyskinesias but also caused bradykinesia, ataxia, dystonia and myoclonic jerks. GAG and GVG reduced dyskinesias to a lesser extent and with fewer side effects. Whether the observed antidyskinetic effect is secondary to the concomitant general toxic effects or if these drugs have a specific antidyskinetic action remains an open question.

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Gamma-acetylenic GABA in tardive dyskinesia

Cited by 10 publications

References 0 publications

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

Tiagabine inhibits haloperidol-induced oral dyskinesias in rats

GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

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