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Updated: Jun 21, 2026
Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice
Published on: January 25, 2022
Spinal microglial expression and mechanical hypersensitivity in a postoperative pain model: comparison with a
Naomi Ito1, Hideaki Obata, Shigeru Saito
1Department of Anesthesiology, Gunma University Graduate School of Medicine, Showa, Maebashi, Gunma, Japan.
Background:
Postoperative pain control contributes to quality of life. Activation of spinal cord microglia after peripheral nerve injury contributes to mechanical hypersensitivity. The contribution of spinal cord microglia to hypersensitivity after surgery, however, is not well understood. Here, the authors evaluated whether inhibition of spinal microglia reduced postoperative mechanical hypersensitivity, and if so, whether the effect differed from that in a rat neuropathic pain model.
Methods:
Male Sprague-Dawley rats underwent either unilateral plantar hind paw incision (postoperative pain model) or L5 spinal nerve transection (neuropathic pain model), and the development of mechanical hypersensitivity was assessed using von Frey filaments. The microglial inhibitor minocycline was intraperitoneally administered daily for either 3 or 7 days. Spinal microglial activation was evaluated by OX42 immunohistochemistry. We also tested the effect of intrathecal administration of a p38 mitogen-activated protein kinase inhibitor, SB203580.
Results:
In the postoperative pain model, minocycline did not suppress mechanical hypersensitivity, but did inhibit an increase in spinal OX42 expression. In contrast, in the neuropathic pain model, minocycline reduced mechanical hypersensitivity in a dose-related manner and inhibited spinal OX42 expression. SB203580 attenuated hypersensitivity in the neuropathic pain model, but not in the postoperative pain model.
Conclusions:
The results of the present study suggest that spinal OX42 expression has a more important role in the development of neuropathic pain than in postoperative pain, and that an increase in spinal OX42 expression does not contribute to postoperative mechanical hypersensitivity.
Insights
Spinal microglia activation does not drive postoperative pain hypersensitivity. Inhibition of spinal microglia effectively treats neuropathic pain but not postsurgical pain in rats.
Area of Science:
- Neuroscience
- Pain Research
- Immunology
Background:
- Effective postoperative pain management is crucial for patient recovery and quality of life.
- Spinal cord microglia activation is implicated in neuropathic pain hypersensitivity.
- The role of spinal microglia in postsurgical pain remains unclear.
Purpose of the Study:
- To investigate if inhibiting spinal microglia reduces postoperative mechanical hypersensitivity.
- To compare the effects of microglial inhibition in postoperative pain versus neuropathic pain models.
- To assess the involvement of p38 mitogen-activated protein kinase (MAPK) signaling.
Main Methods:
- Rats underwent either hind paw incision (postoperative) or L5 spinal nerve transection (neuropathic).
- Mechanical hypersensitivity was measured using von Frey filaments.
- Minocycline (microglial inhibitor) or SB203580 (p38 MAPK inhibitor) were administered.
Main Results:
- Minocycline did not reduce postoperative hypersensitivity but inhibited spinal OX42 expression.
- Minocycline dose-dependently reduced neuropathic hypersensitivity and spinal OX42 expression.
- SB203580 attenuated neuropathic hypersensitivity but not postoperative hypersensitivity.
Conclusions:
- Spinal OX42 expression plays a greater role in neuropathic pain than postoperative pain.
- Increased spinal OX42 expression does not contribute to postoperative mechanical hypersensitivity.
- Microglial inhibition is effective for neuropathic pain, not postoperative pain.
