A novel method to quantify histochemical changes throughout the mediolateral axis of the substantia gelatinosa after spared nerve injury: characterization with TRPV1 and substance P.

A novel method to quantify histochemical changes throughout the mediolateral axis of the substantia gelatinosa after spared nerve injury: characterization with TRPV1 and substance P.
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DOI:
10.1016/j.jpain.2009.09.008
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发表时间:
2010-04
期刊:
The journal of pain
影响因子:
--
通讯作者:
Taylor BK
Taylor BK
中科院分区:
其他
文献类型:
--
作者:
Corder G;Siegel A;Intondi AB;Zhang X;Zadina JE;Taylor BK

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神经损伤显著增加或减少脊髓背角的蛋白表达。这些变化的空间分布是否局限于损伤神经的中枢神经支配区域,或者是否可以扩散到背角的邻近区域,目前尚不清楚。为了解决这个问题,我们开发了一种简单的计算机软件辅助方法,在胫骨和腓总神经(因此保留腓总神经分支,避免神经损伤,SNI),胫骨神经或腓总神经和腓总神经横断2周后,精确区分和有效量化横跨背角中外侧轴的免疫组织化学染色模式。利用硫胺素单磷酸酶(TMP)组织化学,我们确定胫骨神经、腓总神经、腓肠神经和后皮神经的中央末梢分别占据明胶质的内侧35%、内侧-中央20%、中央-外侧20%和外侧25%。然后,我们使用这些计算结果表明,SNI降低了L4背角胫骨和腓神经支配区域内SP和TRPV1免疫反应性的表达,而未损伤的腓肠部分的表达没有改变。我们得出结论,sni诱导的背角中央末端SP和TRPV1的损失仅限于受损纤维。我们的新方法可以直接比较受伤和未受伤的背角末梢,以便更好地了解它们在慢性疼痛机制中的相对贡献。
Nerve injury dramatically increases or decreases protein expression in the spinal cord dorsal horn. Whether the spatial distribution of these changes is restricted to the central innervation territories of injured nerves or could spread to adjacent territories in the dorsal horn is not understood. To address this question, we developed a simple computer software-assisted method to precisely distinguish and efficiently quantify immunohistochemical staining patterns across the mediolateral axis of the dorsal horn 2 wk after transection of either the tibial and common peroneal nerves (thus sparing the sural branch, spared nerve injury, SNI), the tibial nerve, or the common peroneal and sural nerves. Using thiamine monophosphatase (TMP) histochemistry, we determined that central terminals of the tibial, common peroneal, sural, and posterior cutaneous nerves occupy the medial 35%, medial-central 20%, central-lateral 20%, and lateral 25% of the substantia gelatinosa, respectively. We then used these calculations to show that SNI reduced the expression of SP and TRPV1 immunoreactivity within the tibial and peroneal innervation territories in the L4 dorsal horn, without changing expression in the uninjured, sural sector. We conclude that SNI-induced loss of SP and TRPV1 in central terminals of dorsal horn is restricted to injured fibers. Our new method enables direct comparison of injured and uninjured terminals in the dorsal horn so as to better understand their relative contributions to mechanisms of chronic pain.
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