Spinally administered α₂-adrenergic agonists show analgesic effects in normal and neuropathic states. Their effects are mediated via α₂-adrenoceptors. Plasticity of nervous system after nerve injury can change the expressions of the related receptors in spinal cord. The expression of α₂-adrenoceptor subtypes in spinal cord and the effect of chronic systemic administration of tramadol was probed in neuropathic rat pain model.

Spinally administered α₂-adrenergic agonists show analgesic effects in normal and neuropathic states. Their effects are mediated via α₂-adrenoceptors. Plasticity of nervous system after nerve injury can change the expressions of the related receptors in spinal cord. The expression of α₂-adrenoceptor subtypes in spinal cord and the effect of chronic systemic administration of tramadol was probed in neuropathic rat pain model.

Sprague-Dawley rats were prepared to make neuropathic pain model by L5 and L6 spinal nerve ligation. Withdrawal threshold for tactile allodynia was evaluated with von Frey hair throughout experiment. Tramadol (15 mg/kg) or equivalent volume of saline was injected intraperitoneally twice a day for 21 days. In the 14th day and 21st day, allodynia and the systemic effect of tramadol was measured and compared with control group. At the 21st day, rat spinal cords were harvested and the expression of α₂-adrenoceptor subtypes were measured and compared with real time PCR.

Chronic administration of tramadol did not improve the allodynia nor the effect of tramadol in spinal nerve ligation model. The mRNA of α_2A-adrenoceptor in nerve injury site decreased compared to controlateral site. The mRNA of α_2C-adrenoceptor subtype in nerve injury rat decreased compared with normal animal, and chronic administration of tramadol increased it compared to saline group.

Rats with neuropathic pain by spinal nerve ligation showed the expression of α₂-adrenoceptors subtypes in spinal cord, and chronic systemic administration of tramadol may influence the expression of α₂-adrenoceptors subtypes.