The Role of Transient Receptor Potential Vanilloid 1 Receptor in Desipramine Induced Analgesic Effect in Diabetic Mice

Hyperalgesia is one of the debilitating complications of diabetes. The thermal allodynia and hyperalgesia in diabetic mice may be due to the hyperactivity of C-fiber in the spinal cord. Transient receptor potential vanilloid type 1 (TRPV1) present in spinal cord and activation of C-fibre may involve in hyperalgesia in diabetic mice. Desipramine is one of the tricyclic antidepressants, effective in diabetic neuropathy. The intravenous administration of desipramine depresses the C-fibre reflex that will involve in activation of convergent neurons of the spinal cord. Thus, the present study was carried out to find out the role of TRPV1 in desipramine induced analgesic effect in diabetic hyperalgesia. Mice were administered capsaicin (1 mg kg), capsazepine (15 mg kg), desipramine (10 mg kg) from day 4 to day 11 after induction of diabetes and the nociceptive threshold was measured in terms of reaction time, tail flick latency and tail withdrawal latency. The nociceptive threshold was significantly (p < 0.05) lower in diabetic mice as compared with control group. Capsaicin produced a significant (p < 0.05) decrease in reaction time, tail flick latency and tail withdrawal latency as compare to diabetic group. Desipramine caused a significant (p < 0.05) increase in nociceptive threshold in diabetic group as well as capsaicin treated diabetic group. It was concluded that desipramine produced analgesic effect in diabetic hyperalgesia and TRPV1 might be involved in desipramine induced analgesic effect.