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神经元-神经胶质信号在调控大鼠视网膜血管张力中的作用。

Role of Neuron⁻Glia Signaling in Regulation of Retinal Vascular Tone in Rats.

机构信息

Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan.

出版信息

Int J Mol Sci. 2019 Apr 20;20(8):1952. doi: 10.3390/ijms20081952.

DOI:10.3390/ijms20081952
PMID:31010057
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6514555/
Abstract

The interactions between neuronal, glial, and vascular cells play a key role in regulating blood flow in the retina. In the present study, we examined the role of the interactions between neuronal and glial cells in regulating the retinal vascular tone in rats upon stimulation of retinal neuronal cells by intravitreal injection of N-methyl-d-aspartic acid (NMDA). The retinal vascular response was assessed by measuring the diameter of the retinal arterioles in the in vivo fundus images. Intravitreal injection of NMDA produced retinal vasodilation that was significantly diminished following the pharmacological inhibition of nitric oxide (NO) synthase (nNOS), loss of inner retinal neurons, or intravitreal injection of glial toxins. Immunohistochemistry revealed the expression of nNOS in ganglion and calretinin-positive amacrine cells. Moreover, glial toxins significantly prevented the retinal vasodilator response induced by intravitreal injection of NOR3, an NO donor. Mechanistic analysis revealed that NO enhanced the production of vasodilatory prostanoids and epoxyeicosatrienoic acids in glial cells in a ryanodine receptor type 1-dependent manner, subsequently inducing the retinal vasodilator response. These results suggest that the NO released from stimulated neuronal cells acts as a key messenger in neuron-glia signaling, thereby causing neuronal activity-dependent and glial cell-mediated vasodilation in the retina.

摘要

神经元、神经胶质细胞和血管细胞之间的相互作用在调节视网膜血流中起着关键作用。在本研究中，我们研究了神经元和神经胶质细胞之间相互作用在调节大鼠视网膜血管张力中的作用，方法是通过向玻璃体腔注射 N-甲基-D-天冬氨酸（NMDA）刺激视网膜神经元细胞。通过测量活体眼底图像中视网膜小动脉的直径来评估视网膜血管反应。玻璃体腔注射 NMDA 可引起视网膜血管扩张，而一氧化氮（NO）合酶（nNOS）的药理学抑制、内视网膜神经元的丧失或玻璃体内注射神经胶质毒素可显著减少这种扩张。免疫组织化学显示 nNOS 在神经节细胞和 calretinin 阳性无长突细胞中表达。此外，神经胶质毒素可显著预防玻璃体腔注射 NO 供体 NOR3 引起的视网膜血管扩张反应。机制分析表明，NO 以ryanodine 受体 1 依赖性方式增强了神经胶质细胞中血管扩张性前列腺素和环氧二十碳三烯酸的产生，随后引起视网膜血管扩张反应。这些结果表明，刺激神经元细胞释放的 NO 作为神经元-神经胶质信号传递中的关键信使，从而导致视网膜神经元活动依赖性和神经胶质细胞介导的血管扩张。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e57/6514555/074fc06bdd6b/ijms-20-01952-g009.jpg
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