[Effect of the quantal composition, membrane potential and cholinoreceptor density on the temporal flow of the end plate current in the rat under conditions of acetylcholinesterase inhibition].

Neirofiziologiia = Neurophysiology Pub Date : 1992-01-01
R A Giniatullin, A B Shvetsov
{"title":"[Effect of the quantal composition, membrane potential and cholinoreceptor density on the temporal flow of the end plate current in the rat under conditions of acetylcholinesterase inhibition].","authors":"R A Giniatullin,&nbsp;A B Shvetsov","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The factors determining the decay of multiquantal end plate currents (EPC) were studied in the diaphragm muscle of rat by the comparison of EPC and miniature EPC (MEPC) amplitude--temporal characteristics. The decay of EPC (quantal content 25-100) was 1.2 times slower than the decay of MEPC when AChE was active. The AChE inhibition by armine or neostigmine made this difference 10-100 times higher. In most synapses the decay of multiquantal EPC can be approximated by a sum of two or three exponents. It depended on the quantal content and 3-exponential EPC could be transformed in 2-exponential and later to monoexponential ones if increasing concentration of magnesium ions. A slow component of EPCs (but not of MEPC) decay was highly sensitive to concentration of magnesium ions and had 3 times higher dependence of the membrane potential value than that one of MEPC. The irreversible blocking of receptors by alpha-bungarotoxin (alpha-BuTX) accelerated the decay of MEPC but the decay of multiquantal EPC changed in two phases: it was prolonged at the beginning of alpha-BuTX action followed by its acceleration, but never the time of the decay of EPC had achieved the apparent open time of ACh-activated ionic channels. It is suggested that during the multiquantal EPC generation not only the synchronization of opening but the kinetic of ACh-activated channels is changed, probably by blocking of this channels by high concentrations of endogenous ACh.</p>","PeriodicalId":19121,"journal":{"name":"Neirofiziologiia = Neurophysiology","volume":"24 3","pages":"269-79"},"PeriodicalIF":0.0000,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neirofiziologiia = Neurophysiology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The factors determining the decay of multiquantal end plate currents (EPC) were studied in the diaphragm muscle of rat by the comparison of EPC and miniature EPC (MEPC) amplitude--temporal characteristics. The decay of EPC (quantal content 25-100) was 1.2 times slower than the decay of MEPC when AChE was active. The AChE inhibition by armine or neostigmine made this difference 10-100 times higher. In most synapses the decay of multiquantal EPC can be approximated by a sum of two or three exponents. It depended on the quantal content and 3-exponential EPC could be transformed in 2-exponential and later to monoexponential ones if increasing concentration of magnesium ions. A slow component of EPCs (but not of MEPC) decay was highly sensitive to concentration of magnesium ions and had 3 times higher dependence of the membrane potential value than that one of MEPC. The irreversible blocking of receptors by alpha-bungarotoxin (alpha-BuTX) accelerated the decay of MEPC but the decay of multiquantal EPC changed in two phases: it was prolonged at the beginning of alpha-BuTX action followed by its acceleration, but never the time of the decay of EPC had achieved the apparent open time of ACh-activated ionic channels. It is suggested that during the multiquantal EPC generation not only the synchronization of opening but the kinetic of ACh-activated channels is changed, probably by blocking of this channels by high concentrations of endogenous ACh.

分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
[量子组成、膜电位和胆碱受体密度对乙酰胆碱酯酶抑制条件下大鼠端板电流时间流动的影响]。
通过对大鼠横膈肌多量子终板电流(EPC)和微型终板电流(MEPC)振幅-时间特征的比较,研究了影响大鼠横膈肌多量子终板电流衰减的因素。当AChE有活性时,EPC(量子含量25-100)的衰减速度比MEPC的衰减速度慢1.2倍。甲胺或新斯的明对乙酰胆碱酯酶的抑制作用使这一差异提高10-100倍。在大多数突触中,多量子EPC的衰减可以用两个或三个指数的总和来近似。随着镁离子浓度的增加,3指数型EPC可由2指数型转变为单指数型。EPCs(而非MEPC)的缓慢衰变组分对镁离子浓度高度敏感,对膜电位值的依赖性是MEPC的3倍。甲虫毒素(α - butx)对受体的不可逆阻断加速了MEPC的衰变,但多量子EPC的衰变表现为两个阶段:α - butx作用开始时延长,随后加速,但EPC的衰变时间从未达到ach活化离子通道的表观开放时间。这表明,在多量乙酰胆碱生成过程中,乙酰胆碱激活的通道不仅开放的同步性发生了改变,而且动力学也发生了变化,这可能是由于高浓度的内源性乙酰胆碱阻断了这些通道。
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
Dynamic Clamp Analysis of Synaptic Integration in Sympathetic Ganglia. [Viscerosomatic convergence on the lumbar interneurons of the dorsal horn of the spinal cord in cats and rats]. [Relationship between the crystal lattice structure and the biological action of some agonists of amino acid receptors]. [Mechanisms of calcium current decay acceleration induced by cyclic AMP]. [Influence of phosphorylation on the functional properties of the sodium channel reconstructed in an artificial membrane].
×
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