Adrenergic sensitivity of the sensory receptors modulating mechanical allodynia in a rat neuropathic pain model

This study focuses on changes in adrenergic sensitivity in untransected sen sory axons that innervate an area of skin made neuropathic by transection o f neighboring nerves. The segmental nerve injury model is favorable for thi s since all axons in the L5 and L6 nerves are transected whereas the L4 axo ns are intact. Earlier findings are that pain behaviors develop after this injury and that these beahviors are ameliorated by sympathectomy, The prese nt study shows that behavior indicating mechanical allodynia can be rekindl ed after sympathectomy by intradermal norepinephrine and alpha-2 but not al pha-1 adrenergic ligands and the rekindling can be blocked by alpha-2 but n ot alpha-1 adrenergic antagonists. By contrast neither intradermal norepine phrine nor other adrenergic agonists or antagonists have any demonstrable e ffects in the normal or after either neuropathic surgery or sympathectomy a lone. These data suggest that the combination of neuropathic surgery and sy mpathectomy results in an upregulation of active alpha-2 adrenergic recepto rs on the undamaged sensory axons that provide the remaining sensory innerv ation to a neuropathic area partially denervated by segmental nerve lesions . These changes on undamaged axons presumably compliment similar changes on the transected axone and, thus play a role in the development of neuropath ic pain. (C) 1999 International Association for the Study of Pain. Publishe d by Elsevier Science B.V.