Volume 4, Issue 1 (Spring and Summer 2000)                   Physiol Pharmacol 2000, 4(1): 85-94 | Back to browse issues page

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Valizadeh S, Zarrindast M R. The role of GABAB receptors in imipramine-induced antinociception in experimental model of neuropathic pain. Physiol Pharmacol. 2000; 4 (1) :85-94
URL: http://ppj.phypha.ir/article-1-236-en.html
Abstract:   (12286 Views)
This study was designed to investigate the role of GABAB receptor agents on imipramine-induced antinociception in ligated and non-ligated mice using hot-plate test. The data showed that different doses of morphine (3, 6, and 9 mg/kg) induced a dose-dependent antinociception in ligated and non-ligated mice. However, the opioid response was decreased in ligated animals. Intracerebroventricular (i.c.v.) administration of imipramine (5, 10, 20, and 40 µg/mouse) did not induce antinociception in either non-ligated or ligated mice. However, the induced response in the ligated mice was less than that induced in the non-ligated mice. Intraperitoneal (i.p.) administration of imipramine (10, 20, 30, and 40 mg/kg) induced antinociception in both ligated and non-ligated mice. The responses to the drug were not significantly different in the two groups. Administration of baclofen either i.c.v. (0.125, 0.25, and 0.5 µg/mouse) or i.p. (0.5, 1,2, and 4 mg/kg) induced antinociception. The response to the drug was not significantly different in ligated and non-ligated mice. Intracerebroventricular administration of a lower dose of baclofen (0.125 µg/mouse) with different doses of imipramine (2.5, 5, and 10 mg/kg) potentiated the response to imipramine. This effect was reduced by i.c.v. injection of GABAB receptor antagonist, CGP35348 [P-(3-aminopropyl)-p-diethoxymethyl- phosphinic acid] at a dose of 20 µg/mouse. The higher dose of antagonist (20 µg /mouse) also decreased the response induced by baclofen or imipramine. CGP35348 itself (2.5, 5, 10, and 20 µg/mouse) induced a dose-dependent antinociception with no significant difference in the ligated and non-ligated mice. It is concluded that a GABA receptor mechanism(s) may modulate the antidepressant-induced antinociception.
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