Baclofen induces catatonia in rats

It is suggested that baclofen-induced catatonia was susceptible to reversal by homotaurine and delta-amino-n-valeric acid, and this effect could be mediated through GABAB receptors, which is known to bind to a subpopulation of GABA receptors.

Abstract

Baclofen (10 and 20 mg/kg, i.p.) induced catatonia in rats within 10 min of its administration and the effect lasted for 3 hr. Muscimol (100 ng i.c.v. or 1 mg/kg, i.p.) as well as GABA (5 micrograms i.c.v.) potentiated the effect without producing any effect per se. Bicuculline, bromocriptine and scopolamine failed to modify the catatonia induced by baclofen, thereby ruling out the involvement of GABAA receptors, dopaminergic and cholinergic mechanisms. However, GABAB receptor antagonists, such as homotaurine and delta-amino-n-valeric acid, reversed the catatonia induced by baclofen in rats. Since baclofen is known to bind to a subpopulation of GABA receptors (bicuculline-insensitive) and baclofen-induced catatonia was susceptible to reversal by homotaurine and delta-amino-n-valeric acid, it is suggested that this effect could be mediated through GABAB receptors.