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大鼠眼部强光刺激后三叉神经节中降钙素基因相关肽、神经元型一氧化氮合酶及磷酸化细胞外信号调节激酶1/2的上调

Upregulation of calcitonin gene-related peptide, neuronal nitric oxide synthase, and phosphorylated extracellular signal-regulated kinase 1/2 in the trigeminal ganglion after bright light stimulation of the eye in rats.

作者信息

Okada Shinji, Saito Hiroto, Matsuura Yutaka, Mikuzuki Lou, Sugawara Shiori, Onose Hiroki, Asaka Junichi, Ohara Kinuyo, Lee Jun, Iinuma Toshimitsu, Katagiri Ayano, Iwata Koichi

机构信息

Department of Complete Denture Prosthodontics, Nihon University School of Dentistry.

Department of Physiology, Nihon University School of Dentistry.

出版信息

J Oral Sci. 2019;61(1):146-155. doi: 10.2334/josnusd.18-0031.

DOI:10.2334/josnusd.18-0031
PMID:30918211
Abstract

Bright light stimulation of the eye activates trigeminal subnucleus caudalis (Vc) neurons in rats. Sensory information is conveyed to the Vc via the trigeminal ganglion (TG). Thus, it is likely that TG neurons respond to photic stimulation and are involved in photic hypersensitivity. However, the mechanisms underlying this process are unclear. Therefore, the hypothesis in this study is bright light stimulation enhances the excitability of TG neurons involved in photic hypersensitivity. Expressions of calcitonin gene-related peptide (CGRP) and neuronal nitric oxide synthase (nNOS) were significantly higher in TG neurons from 5 min to 12 h after photic stimulation of the eye. Phosphorylation of extracellular signal-regulated kinase1/2 (pERK1/2) was enhanced in TG neurons within 5 min after photic stimulation, while pERK1/2 immunoreactivity in satellite glial cells (SGCs) persisted for more than 12 h after the stimulus. Activation of SGCs was observed from 5 min to 2 h. Expression of CGRP, nNOS, and pERK1/2 was observed in small and medium TG neurons, and activation of SGCs and pERK1/2-immunoreactive SGCs encircling large TG neurons was accelerated after stimulation. These results suggest that upregulation of CGRP, nNOS, and pERK1/2 within the TG is involved in photic hypersensitivity.

摘要

眼部的强光刺激可激活大鼠三叉神经尾侧亚核(Vc)神经元。感觉信息通过三叉神经节(TG)传递至Vc。因此,TG神经元可能对光刺激产生反应并参与光过敏反应。然而,这一过程的潜在机制尚不清楚。因此,本研究的假设是强光刺激增强了参与光过敏反应的TG神经元的兴奋性。眼部光刺激后5分钟至12小时,TG神经元中降钙素基因相关肽(CGRP)和神经元型一氧化氮合酶(nNOS)的表达显著升高。光刺激后5分钟内,TG神经元中细胞外信号调节激酶1/2(pERK1/2)的磷酸化增强,而卫星神经胶质细胞(SGCs)中的pERK1/2免疫反应性在刺激后持续超过12小时。在5分钟至2小时观察到SGCs的激活。在中小型TG神经元中观察到CGRP、nNOS和pERK1/2的表达,刺激后,围绕大型TG神经元的SGCs和pERK1/2免疫反应性SGCs的激活加速。这些结果表明,TG内CGRP、nNOS和pERK1/2的上调参与了光过敏反应。

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