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[细胞内信使及其在视网膜缝隙连接中的作用]

[Intracellular messengers and their roles in retinal gap junctions].

作者信息

Miyachi E

机构信息

Department of Physiology, Fujita Health University School of Medicine, Aichi, Japan.

出版信息

Yakubutsu Seishin Kodo. 1992 Jun;12(3):129-34.

PMID:1329400
Abstract

Intracellular injection of cAMP or cGMP into retinal horizontal cells blocked the gap junctions between the cells. Similar results were obtained when L-arginine was injected into the cells. L-Arginine is a substrate of nitric oxide (NO) which is believed to activate soluble guanylate cyclase to produce cGMP. The endothelium-derived relaxing factor (EDRF) in the blood vessels has been identified as NO. With respect to the nervous systems, production of NO and its synthase have been found in the brain, and NO has been discussed in relation to such phenomena as synaptic plasticity, long-term potentiation, and development. The decoupling effect of L-arginine suggests the presence of the L-arginine: NO: cGMP pathway in the retina as well. Before injection of cAMP, cGMP or L-arginine, the applied current leaked through the gap junctions. After the injection, the horizontal cells could be easily polarized by intracellular current injection, and the synaptic mechanisms were analyzed by measuring I-V curves. In luminosity-type (H1) horizontal cells, the reversal potential of light responses was estimated at about 0 mV. In addition, conductance decreases were detected during illumination. These findings support the widely accepted hypothesis that glutamate is released from the photoreceptors in darkness. In chromaticity-type cells (H2 and H3 cells), the reversal potentials of light responses were about 0 mV, suggesting that the ionic mechanisms of synaptic transmission are common among horizontal cell types.

摘要

向视网膜水平细胞内注射环磷酸腺苷(cAMP)或环磷酸鸟苷(cGMP)会阻断细胞间的缝隙连接。向细胞内注射L-精氨酸时也得到了类似结果。L-精氨酸是一氧化氮(NO)的底物,据信它能激活可溶性鸟苷酸环化酶以产生cGMP。血管中的内皮源性舒张因子(EDRF)已被确定为NO。在神经系统方面,已在大脑中发现了NO及其合酶的产生,并且已经讨论了NO与诸如突触可塑性、长时程增强和发育等现象的关系。L-精氨酸的解偶联效应表明视网膜中也存在L-精氨酸:NO:cGMP途径。在注射cAMP、cGMP或L-精氨酸之前,施加的电流会通过缝隙连接泄漏。注射后,通过细胞内电流注入可以很容易地使水平细胞极化,并通过测量I-V曲线来分析突触机制。在亮度型(H1)水平细胞中,光反应的反转电位估计约为0 mV。此外,在光照期间检测到电导降低。这些发现支持了广泛接受的假说,即在黑暗中谷氨酸从光感受器释放。在色度型细胞(H2和H3细胞)中,光反应的反转电位约为0 mV,这表明突触传递的离子机制在水平细胞类型中是常见的。

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