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Is GABAA receptor involved in trigeminal nociceptive transmission?

GABAA 受体是否参与三叉神经伤害性传递？

基本信息

批准号：
20390511
负责人：
SEO Kenji
金额：
$ 11.23万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2008
资助国家：
日本
起止时间：
2008 至 2010
项目状态：
已结题

项目摘要

Introduction ; This project aimed to investigate the possible involvement of GABAA receptor mediated nociceptive modulation in the spinal or trigeminal dorsal horn. We used PRIP-1, PRIP-2 double knockout mice (DKO) which deficits some GAGAA receptor function.Method and results : Immnunohistochemical study exhibited a complete deficit in γ2 subunit of GABAA receptor on cell surface of the superficial and deep magnocellular layers in spinal cord of DKO mice. The MAC of wild or DKO animal was 1.36±0.04% (n=10) or 1.07±0.01% (n=10), respectively (Student's t-test, p<0.001). These results suggest that the stimulation of γ2 subunit might did not induce anti-nociceptive effect. Thirdly, spatial and temporal propagation of membrane potential and the changes in the intra- cellular calcium concentration in the slice of medulla exhibited the similar propagation between in the wild and DKO animals and furthermore a perfusion of the highly-selective GABAA receptor agonist muscimol did not induce any difference in these propagation features. The preconditioning by BDNF induced some difference in afferent stimulation induced changes in membrane potential propagation under muscimol perfusion.Conclusion ; these results suggest that GABAA receptor does not have any significant role in modulation of nociceptive transmission in normal condition but some stimuli induce BDNF releasing might have some modulating effect on this transmission feature.

介绍 ;该项目旨在研究 GABAA 受体介导的伤害性调节在脊髓或三叉神经背角中的可能参与。我们使用PRIP-1、PRIP-2双基因敲除小鼠（DKO），其部分GAGAA受体功能缺陷。方法和结果：免疫组织化学研究显示DKO小鼠脊髓浅层和深层大细胞层细胞表面的GABAA受体γ2亚基完全缺陷。野生动物或 DKO 动物的 MAC 分别为 1.36±0.04% (n=10) 或 1.07±0.01% (n=10)（学生 t 检验，p<0.001）。这些结果表明γ2亚基的刺激可能不会引起抗伤害作用。第三，膜电位的空间和时间传播以及髓质切片中细胞内钙浓度的变化在野生动物和DKO动物中表现出相似的传播，此外，灌注高选择性GABAA受体激动剂蝇蕈醇不会引起这些传播特征的任何差异。 BDNF预处理引起了传入刺激诱导的蝇蕈醇灌注下膜电位传播变化的一些差异。这些结果表明，在正常情况下，GABAA 受体在调节伤害性传递中没有任何显着作用，但某些刺激诱导 BDNF 释放可能对此传递特征有一定的调节作用。