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眶下神经炎性压迫(TIC)诱导的口面神经性疼痛小鼠模型。

Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve.

机构信息

Department of Physiology MS-508, College of Medicine, University of Kentucky, Lexington, KY 40536-0298, USA.

出版信息

Mol Brain. 2012 Dec 28;5:44. doi: 10.1186/1756-6606-5-44.

Abstract

BACKGROUND

Trigeminal neuropathic pain attacks can be excruciating for patients, even after being lightly touched. Although there are rodent trigeminal nerve research models to study orofacial pain, few models have been applied to studies in mice. A mouse trigeminal inflammatory compression (TIC) model is introduced here which successfully and reliably promotes vibrissal whisker pad hypersensitivity.

RESULTS

The chronic orofacial neuropathic pain model is induced after surgical placement of chromic gut suture in the infraorbital nerve fissure in the maxillary bone. Slight compression and chemical effects of the chromic gut suture on the portion of the infraorbital nerve contacted cause mild nerve trauma. Nerve edema is observed in the contacting infraorbital nerve bundle as well as macrophage infiltration in the trigeminal ganglia. Centrally in the spinal trigeminal nucleus, increased immunoreactivity for an activated microglial marker is evident (OX42, postoperative day 70). Mechanical thresholds of the affected whisker pad are significantly decreased on day 3 after chromic gut suture placement, persisting at least 10 weeks. The mechanical allodynia is reversed by suppression of microglial activation. Cold allodynia was detected at 4 weeks.

CONCLUSIONS

A simple, effective, and reproducible chronic mouse model mimicking clinical orofacial neuropathic pain (Type 2) is induced by placing chromic gut suture between the infraorbital nerve and the maxillary bone. The method produces mild inflammatory compression with significant continuous mechanical allodynia persisting at least 10 weeks and cold allodynia measureable at 4 weeks.

摘要

背景

三叉神经病理性疼痛发作会令患者感到剧痛,甚至在被轻触后也会如此。虽然有研究啮齿动物三叉神经的疼痛模型,但很少有模型适用于研究小鼠的疼痛。本文引入了一种小鼠三叉神经炎性压迫(TIC)模型,该模型成功且可靠地促进了触须垫的超敏反应。

结果

在眶下神经裂上颌骨中的铬肠缝线手术后,慢性口面神经性疼痛模型被诱导。铬肠缝线对接触的眶下神经部分的轻微压迫和化学作用导致轻度神经创伤。接触的眶下神经束中观察到神经水肿以及三叉神经节中的巨噬细胞浸润。在脊髓三叉神经核中,活化的小胶质细胞标志物的免疫反应增强(OX42,术后第 70 天)。铬肠缝线放置后第 3 天,受影响的触须垫的机械阈值显著降低,至少持续 10 周。通过抑制小胶质细胞活化可逆转机械性痛觉过敏。在第 4 周检测到冷感觉过敏。

结论

通过在眶下神经和上颌骨之间放置铬肠缝线,诱导出一种简单、有效且可重复的模拟临床口面神经性疼痛(2 型)的慢性小鼠模型。该方法产生轻度炎症性压迫,具有显著的持续机械性痛觉过敏,至少持续 10 周,并且可在第 4 周测量到冷感觉过敏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab2b/3563613/0e1018bdf0a9/1756-6606-5-44-1.jpg

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