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改良 spared nerve injury 模型在小鼠神经病理性疼痛中的应用。

Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice.

机构信息

Department of Pain Management, Xuanwu Hospital, Capital Medical University; Department of Anesthesia and Perioperative Care, University of California San Francisco.

Department of Pain Management, Xuanwu Hospital, Capital Medical University.

出版信息

J Vis Exp. 2022 Jan 25(179). doi: 10.3791/63362.


DOI:10.3791/63362
PMID:35156658
Abstract

Spared nerve injury (SNI) is an animal model that mimics the cardinal symptoms of peripheral nerve injury for studying the molecular and cellular mechanism of neuropathic pain in mice and rats. Currently, there are two types of SNI model, one to cut and ligate the common peroneal and the tibial nerves with intact sural nerve, which is defined as SNIs in this study, and another to cut and ligate the common peroneal and the sural nerves with intact tibial nerve, which is defined as SNIt in this study. Because the sural nerve is purely sensory whereas the tibial nerve contains both motor and sensory fibers, the SNIt model has much less motor deficit than the SNIs model. In the traditional SNIt mouse model, the common peroneal and the sural nerves are cut and ligated separately. Here a modified SNIt surgery method is described to damage both common peroneal and sural nerves with only one ligation and one cut with a shorter procedure time, which is easier to perform and reduces the potential risk of stretching the sciatic or tibial nerves, and produces similar mechanical hypersensitivity as the traditional SNIt model.

摘要

spared nerve injury (SNI) 是一种模拟周围神经损伤主要症状的动物模型,可用于研究小鼠和大鼠神经病理性疼痛的分子和细胞机制。目前,有两种类型的 SNI 模型,一种是在保留完整腓肠神经的情况下同时切断和结扎腓总神经和胫神经,本研究中定义为 SNIs;另一种是在保留完整胫神经的情况下同时切断和结扎腓总神经和腓肠神经,本研究中定义为 SNIt。由于腓肠神经纯粹是感觉神经,而胫神经既有运动神经纤维又有感觉神经纤维,因此 SNIt 模型的运动功能障碍比 SNIs 模型小得多。在传统的 SNIt 小鼠模型中,腓总神经和腓肠神经是分别切断和结扎的。本文描述了一种改良的 SNIt 手术方法,只需一次结扎和一次切断即可同时损伤腓总神经和腓肠神经,手术时间更短,操作更简单,降低了对坐骨神经或胫神经拉伸的潜在风险,并产生与传统 SNIt 模型相似的机械性超敏反应。

相似文献

[1]
Modified Spared Nerve Injury Surgery Model of Neuropathic Pain in Mice.

J Vis Exp. 2022-1-25

[2]
A mouse model of sural nerve injury-induced neuropathy: gabapentin inhibits pain-related behaviors and the hyperactivity of wide-dynamic range neurons in the dorsal horn.

J Pharmacol Sci. 2009-4

[3]
Spared nerve injury: an animal model of persistent peripheral neuropathic pain.

Pain. 2000-8

[4]
Topography and time course of changes in spinal neuropeptide Y immunoreactivity after spared nerve injury.

Neuroscience. 2009-10-30

[5]
The spared nerve injury (SNI) model of induced mechanical allodynia in mice.

J Vis Exp. 2011-8-18

[6]
Antiallodynic Effects of Endomorphin-1 and Endomorphin-2 in the Spared Nerve Injury Model of Neuropathic Pain in Mice.

Anesth Analg. 2017-12

[7]
Association between extracellular signal-regulated kinase expression and the anti-allodynic effect in rats with spared nerve injury by applying immediate pulsed radiofrequency.

BMC Anesthesiol. 2015-6-16

[8]
Sural hypersensitivity after nerve transection depends on anatomical differences in the distal tibial nerve of mice and rats.

Ann Anat. 2023-2

[9]
Sex-Dependent Reduction in Mechanical Allodynia in the Sural-Sparing Nerve Injury Model in Mice Lacking Merkel Cells.

J Neurosci. 2021-6-30

[10]
Analgesic effect of a cholinergic agonist (carbachol) in a sural nerve ligation-induced hypersensitivity mouse model.

Neurol Res. 2024-6

引用本文的文献

[1]
Environmental enrichment for neuropathic pain via modulation of neuroinflammation.

Front Mol Neurosci. 2025-3-21

[2]
Visualizing the modulation of neurokinin 1 receptor-positive neurons in the superficial dorsal horn by spinal cord stimulation in vivo.

Pain. 2025-2-1

[3]
Enhancing spinal cord stimulation-induced pain inhibition by augmenting endogenous adenosine signalling after nerve injury in rats.

Br J Anaesth. 2024-4

[4]
A humanized chemogenetic system inhibits murine pain-related behavior and hyperactivity in human sensory neurons.

Sci Transl Med. 2023-10-4

[5]
Diagnosis and Management of Neuropathic Pain in Spine Diseases.

J Clin Med. 2023-2-9

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