Kasture S B, Mandhane S N, Chopde C T
M. V. P. Samaj's College of Pharmacy, Nashik, India.
Neuropharmacology. 1996 May;35(5):595-8. doi: 10.1016/0028-3908(96)84629-6.
Baclofen, a GABAB receptor agonist can induce catatonia in rats. This catatonia may serve as a tool for the study of GABAB receptor function. Reciprocal interactions between serotonin (5-HT) and GABAB receptors in the CNS are known to occur. In the present study we examined the effect of various agents that influence serotonergic neurotransmission on baclofen-induced catatonia in rats. The catatonia was rated by means of a scoring method, according to the severity of motor symptoms produced by baclofen (10-15 mg/kg, i.p.). All serotonergic drugs were injected intraperitoneally 30 min prior to baclofen, except the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA), which was injected 72 and 48 hr prior to baclofen. The 5-HT releaser fenfluramine (10 mg/kg) and the uptake inhibitor fluoxetine (10 mg/kg) reversed, whereas the 5-HT1A agonist buspirone (3 mg/kg) potentiated baclofen-induced catatonia. The 5-HT synthesis inhibitor PCPA (150 x 2 mg/kg), the non-specific 5-HT antagonist cyproheptadine (5 mg/kg), the 5-HT1A/1B antagonist pindolol (3 mg/kg) and the 5-HT2 antagonist sulpiride (20 mg/kg) enhanced baclofen-induced catatonia. It is concluded that the manipulations of central serotonergic mechanisms modulate baclofen-induced catatonia.
