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

• Published in: Neuroscience letters Vol. 554; pp. 146 - 150
• Main Authors: Leinders, Mathias, Knaepen, Liesbeth, De Kock, Marc, Sommer, Claudia, Hermans, Emmanuel, Deumens, Ronald
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 25.10.2013
• Subjects: Animals; Biomarkers - metabolism; Calcium-Binding Proteins - metabolism; Female; Hyperalgesia - physiopathology; Inflammation; Microfilament Proteins - metabolism; Microglia - metabolism; Nerve injury; Neuralgia - metabolism; Neuralgia - physiopathology; Pain Measurement; Pain mechanisms; Physical Stimulation; Rat; Rats, Sprague-Dawley; Spinal cord; Spinal Cord - metabolism; Spinal Cord - physiopathology; Spinal Nerves - injuries; Time Factors; Touch; Up-Regulation; Spinal cord; Rat; SNT; Nerve injury; CR-3; Inflammation; PWT; Iba-1; Pain mechanisms; ionized calcium-binding adapter protein; spinal nerve transection; paw withdrawal threshold; complement receptor-3
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2013.08.062

•Mechanical pain hypersensitivity resolves at three months after spinal nerve injury.•Up-regulation of spinal microglial Iba-1 expression persists after three months.•Iba-1 expression is higher at 4 weeks than at three months. 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.