Synaptic inputs onto spiking local interneurons in crayfish are depressed by nitric oxide.

H. Aonuma, P. Newland
{"title":"Synaptic inputs onto spiking local interneurons in crayfish are depressed by nitric oxide.","authors":"H. Aonuma, P. Newland","doi":"10.1002/NEU.10081","DOIUrl":null,"url":null,"abstract":"We have analyzed the action of nitric oxide on the synaptic inputs of spiking local interneurons that form part of the local circuits in the terminal abdominal ganglion of the crayfish, Pacifastacus leniusculus. Increasing the availability of NO in the ganglion by bath applying the NO donor SNAP, or the substrate for its synthesis, L-arginine, caused a depression of synaptic inputs onto the interneurons evoked by electrically stimulating mechanosensory neurons in nerve 2 of the terminal ganglion. Conversely, reducing the availability of NO by bath application of an NO scavenger, PTIO, and an inhibitor of nitric oxide synthase, L-NAME, increased the amplitude of the evoked potentials. These results suggest that elevated NO concentration causes a depression of the synaptic inputs to spiking local interneurons. To determine whether these effects could be mediated through an NO/cGMP signaling pathway we bath applied a membrane permeable analogue of cGMP, 8-br-cGMP, which decreased the amplitude of the inputs to the interneurons. Bath application of an inhibitor of soluble guanlylyl cyclase, ODQ, produced an increase in the amplitude of the synaptic inputs. Our results suggest that NO causes a depression of synaptic inputs to spiking local interneurons probably by acting through an NO/cGMP signaling pathway. Moreover, application of NO scavengers modulates the inputs to these interneurons, suggesting that NO is continuously providing a powerful and dynamic means of modulating the outputs of local circuits.","PeriodicalId":16540,"journal":{"name":"Journal of neurobiology","volume":"373 1","pages":"144-55"},"PeriodicalIF":0.0000,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"28","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of neurobiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/NEU.10081","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 28

Abstract

We have analyzed the action of nitric oxide on the synaptic inputs of spiking local interneurons that form part of the local circuits in the terminal abdominal ganglion of the crayfish, Pacifastacus leniusculus. Increasing the availability of NO in the ganglion by bath applying the NO donor SNAP, or the substrate for its synthesis, L-arginine, caused a depression of synaptic inputs onto the interneurons evoked by electrically stimulating mechanosensory neurons in nerve 2 of the terminal ganglion. Conversely, reducing the availability of NO by bath application of an NO scavenger, PTIO, and an inhibitor of nitric oxide synthase, L-NAME, increased the amplitude of the evoked potentials. These results suggest that elevated NO concentration causes a depression of the synaptic inputs to spiking local interneurons. To determine whether these effects could be mediated through an NO/cGMP signaling pathway we bath applied a membrane permeable analogue of cGMP, 8-br-cGMP, which decreased the amplitude of the inputs to the interneurons. Bath application of an inhibitor of soluble guanlylyl cyclase, ODQ, produced an increase in the amplitude of the synaptic inputs. Our results suggest that NO causes a depression of synaptic inputs to spiking local interneurons probably by acting through an NO/cGMP signaling pathway. Moreover, application of NO scavengers modulates the inputs to these interneurons, suggesting that NO is continuously providing a powerful and dynamic means of modulating the outputs of local circuits.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
一氧化氮抑制了小龙虾局部尖峰中间神经元的突触输入。
我们分析了一氧化氮对局部尖峰中间神经元的突触输入的作用,这些神经元构成了小龙虾腹末神经节局部回路的一部分。通过使用一氧化氮供体SNAP或合成一氧化氮的底物l -精氨酸来增加神经节中一氧化氮的可用性,导致电刺激末梢神经节2号神经的机械感觉神经元引起的对中间神经元的突触输入减少。相反,通过使用一氧化氮清除剂PTIO和一氧化氮合酶抑制剂L-NAME来降低一氧化氮的可用性,会增加诱发电位的振幅。这些结果表明,一氧化氮浓度升高导致突触输入抑制局部中间神经元的尖峰。为了确定这些作用是否可以通过NO/cGMP信号通路介导,我们使用了cGMP的膜透性类似物8-br-cGMP,它降低了中间神经元的输入振幅。可溶性胍基酰环化酶(ODQ)抑制剂的大量应用增加了突触输入的振幅。我们的研究结果表明,一氧化氮可能通过一氧化氮/cGMP信号通路抑制局部中间神经元的突触输入。此外,一氧化氮清除剂的应用调节了这些中间神经元的输入,这表明一氧化氮持续地提供了一种强大的动态手段来调节局部电路的输出。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
V Fenstermaker, Y Chen, A Ghosh, R Yuste. Regulation of dendritic length and branching by Semaphorin 3A, Journal of Neurobiology (2004) 58(3) 403–412 Synaptic inputs onto spiking local interneurons in crayfish are depressed by nitric oxide. Remodeling of an identified motoneuron during metamorphosis: central and peripheral actions of ecdysteroids during regression of dendrites and motor terminals. Role of Nova-1 in regulating alpha2N, a novel glycine receptor splice variant, in developing spinal cord neurons. Cloning of the cDNA and mRNA expression of CLRP, a complex leucine repeat protein of the Golgi apparatus expressed by specific neurons of the rat brain.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1