Up-regulation of spinal microglial Iba-1 expression persists after resolution of neuropathic pain hypersensitivity

Abstract

Spinal microglial activation plays a major role in the development of neuropathic pain following peripheral nerve injury. We here provide evidence for an elevated expression of the microglial marker Iba-1 in the lumbar dorsal horn ipsilateral to L5 spinal nerve transection that persists for at least 14 weeks, a time at which mechanical hypersensitivity had fully resolved. Iba-1 expression was, however; significantly lower than at 4 weeks. We therefore conclude that microglia remain partly activated beyond the phase of pain hypersensitivity. Thus, the relation between microglial cells and neuropathic pain outcome is subject to change over time after nerve injury.

Keywords: CR-3; Iba-1; Inflammation; Nerve injury; PWT; Pain mechanisms; Rat; SNT; Spinal cord; complement receptor-3; ionized calcium-binding adapter protein; paw withdrawal threshold; spinal nerve transection.