Neonatal 6-hydroxydopamine lesion of spinal noradrenergic terminals: nociception, clonidine analgesia and spinal alpha two adrenoceptors.

Newborn rats received intraspinal injections of 6-hydroxydopamine to enduringly deplete spinal norepinephrine (NE). When tested in adulthood for pain sensitivity with a hot water-tail immersion procedure, this neonatal spinal NE lesion lowered tail flick latencies of females but not males. It was postulated that this sexually dimorphic sparing or recovery of function reflected the development of denervation supersensitivity for males but not females. Contrary to expectation from such an hypothesis, females, not males, showed exaggerated sensitivity to the analgesic effects of a test dose of clonidine. Furthermore, neither males nor females showed an increased number of spinal cord binding sites for (3H)para-amino-clonidine [(3H)PAC]. These receptor binding data failed to indicate proliferation of the spinal alpha two adrenoceptor in either sex. That the lesioning of spinal NE terminals did not reduce (3H)PAC binding sites suggests that the spinal alpha two adrenoceptor does not reside exclusively on NE terminals. This is consistent with current conclusions concerning the alpha two adrenoceptor in the cerebral cortex.