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一氧化氮介导的螺旋神经节中的环鸟苷酸合成。

Nitric oxide-mediated cGMP synthesis in Helix neural ganglia.

作者信息

Huang S, Kerschbaum H H, Hermann A

机构信息

Department of Animal Physiology, University of Salzburg, Austria.

出版信息

Brain Res. 1998 Jan 12;780(2):329-36. doi: 10.1016/s0006-8993(97)01147-5.

DOI:10.1016/s0006-8993(97)01147-5
PMID:9507180
Abstract

The central nervous system of the mollusc Helix pomatia was stimulated with NO donors sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP) or hydroxylamine, in the presence of a phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine (IBMX). Radioimmunoassay revealed that all of the three NO donors significantly increased cGMP levels by 22-27-fold above basal levels. Compared with controls, strong cGMP immunoreactivity was observed in axons and cytoplasm of the stimulated neurons. About 80% of cGMP-immunoreactive neurons colocalized with NADPH-diaphorase activity. Some glial cells and giant neurons were not stained by NADPH-diaphorase histochemistry but were cGMP-immunoreactive. The results suggest the existence of a NO/cGMP pathway and indicate NO as an intra- and intercellular signaling molecule in the Helix central nervous system.

摘要

在磷酸二酯酶抑制剂1-甲基-3-异丁基黄嘌呤(IBMX)存在的情况下,用一氧化氮供体硝普钠(SNP)、S-亚硝基-N-乙酰青霉胺(SNAP)或羟胺刺激软体动物盖罩大蜗牛的中枢神经系统。放射免疫分析显示,所有这三种一氧化氮供体均使环磷酸鸟苷(cGMP)水平显著升高,比基础水平高出22至27倍。与对照组相比,在受刺激神经元的轴突和细胞质中观察到强烈的cGMP免疫反应性。约80%的cGMP免疫反应性神经元与还原型辅酶II-黄递酶(NADPH-d)活性共定位。一些神经胶质细胞和巨型神经元未被NADPH-d组织化学染色,但具有cGMP免疫反应性。这些结果表明存在一条一氧化氮/cGMP途径,并表明一氧化氮是盖罩大蜗牛中枢神经系统中的一种细胞内和细胞间信号分子。

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引用本文的文献

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Initial studies on the direct and modulatory effects of nitric oxide on an identified central Helix aspersa neuron.关于一氧化氮对已鉴定的中枢大蜗牛神经元的直接和调节作用的初步研究。
Invert Neurosci. 2015;15(1):175. doi: 10.1007/s10158-014-0175-3. Epub 2014 Nov 8.
3
Coordination of rhythm-generating units via NO and extrasynaptic neurotransmitter release.
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J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2010 Aug;196(8):529-41. doi: 10.1007/s00359-010-0541-5. Epub 2010 Jun 18.
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Parasitol Res. 2005 Jan;95(1):22-4. doi: 10.1007/s00436-004-1245-y. Epub 2004 Nov 20.
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