Effects of intrathecal vs. systemic clonidine in treating chronic allodynia-like response in spinally injured rats.

摘要

A chronic pain-like response to innocuous mechanical stimuli (allodynia) was observed in rats after severe spinal cord ischemia, which resembled some painful conditions observed in spinally injured patients. The present studies examined the effects of clonidine, an alpha 2-adrenoceptor agonist, on this allodynia-like response. Intrathecal (i.t.) clonidine dose-dependently relieved allodynia and doses up to 10 micrograms did not induce motor deficits or sedation, but slightly increased systemic blood pressure. The anti-allodynic effect of i.t. clonidine was reversed by the selective alpha 2-adrenoceptor antagonist atipamezole. In contrast, 50 and 100 micrograms/kg intraperitoneal (i.p.) clonidine did not relieve the chronic allodynia, although the higher dose induced some motor deficits and sedation. Allodynic behavior was abolished after 200 micrograms/kg, i.p. clonidine, which, however, caused strong sedative and motor impairment. The present data suggested that spinal, but not systemic, alpha 2-adrenoceptor agonists may have therapeutic value in treating mechanical allodynia in patients with neuropathic pain of spinal origin.