Effect of intraperitoneal clonidine on expression of GAP-43 mRNA in spinal cord in a rat model of chronic neuropathic pain

Abstract

Objective To evaluate the effect of intraperitoneal (IP) clonidine on the expression of GAP-43 mRNA in the spinal cord in a rat model of chronic neuropathic pain. Methods Thirty-six male SD rats weighing 180-220 g were randomly assigned to one of 3 groups (n=12 each) : group Ⅰsham operation (S); group Ⅱ chronic constriction injury (CCI) and group Ⅲ tP clonidine + CCI (CL). The animals were anesthetized with IP 10% chloral hydrate 300 mg/kg. The right sciatic nerve was exposed and 4 ligatures were placed in group CCI and CL. Clonidine 1 mg/kg was given IP immediately after surgery in group CL. Paw-withdrawal threshold (PWT) to thermal and von Frey filament stimulation was measured before (T_0, baseline) and at 3, 7 and 14 days after surgery (T_(1-3)). The animals were then killed. The lumbar segment of the spinal cord was removed for determination of the expression of GAP-43 mRNA. Results The PWT to thermal and mechanical stimulation was significantly reduced at 3 days after surgery (T_1) in group CCI and CL as compared with group S, and was significantly higher at T_2 and T_3 in group CL than in group CCI. The GAP-43 mRNA expression in the spinal cord was significantly increased in group CCI and CL as compared with group S and significantly lower in group CL than in group CCI. Conclusion lntraperitoneal clonidine can inhibit hyperalgesia by reducing the expression of GAP-43 mRNA in the spinal cord in a rat model of chronic neuropathic pain. Key words: Clonidine; GAP-43 protein; Ganglia; spinal; Sciatica