Baclofen-induced Catatonia: Modification by Serotonergic Agents

• Published in: Neuropharmacology 1996-05, Vol.35 (5), p.595-598
• Main Authors: KASTURE, S.B., MANDHANE, S.N., CHOPDE, C.T.
• Format: Article
• Language: English
• Subjects: Animals; baclofen; Baclofen - pharmacology; Biological and medical sciences; catatonia; Catatonia - chemically induced; Drug toxicity and drugs side effects treatment; Fenfluramine - pharmacology; GABA B receptors; Male; Medical sciences; Pharmacology. Drug treatments; Pindolol - pharmacology; Rats; Rats, Wistar; serotonergic neurotransmission; Serotonin Receptor Agonists - pharmacology; Toxicity: nervous system and muscle
• ISSN: 0028-3908; 1873-7064
• DOI: 10.1016/0028-3908(96)84629-6

Baclofen, a GABA B receptor agonist can induce catatonia in rats. This catatonia may serve as a tool for the study of GABA B receptor function. Reciprocal interactions between serotonin (5-HT) and GABA B receptors in the CNS are known to occur. In the present study we examined the effects 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-HT 1A agonist buspirone (3 mg/kg) potentiated baclofen-induced catatonia. The 5-HT synthesis inhibitor PCPA (150 × 2 mg/kg), the non-specific 5-HT antagonist cyproheptadine (5 mg/kg), the 5-HT 1A/1B antagonist pindolol (3 mg/kg) and the 5-HT 2 antagonist sulpiride (20 mg/kg) enhanced baclofen-induced catatonia. It is concluded that the manipulations of central serotonergic mechanisms modulate baclofen-induced catatonia. Copyright © 1996 Elsevier Science Ltd.