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.