• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

羰基氰化物间氯苯腙对蛙运动神经末梢量子递质释放及超微结构的影响

Effects of carbonyl cyanide m-chlorophenylhydrazone on quantal transmitter release and ultrastructure of frog motor nerve terminals.

作者信息

Molgo J, Pecot-Dechavassine M

机构信息

Laboratoire de Neurobiologie Cellulaire et Moléculaire du CNRS, Gif sur Yvette, France.

出版信息

Neuroscience. 1988 Feb;24(2):695-708. doi: 10.1016/0306-4522(88)90362-4.

DOI:10.1016/0306-4522(88)90362-4
PMID:2834667
Abstract

The quantal acetylcholine release and the ultrastructural effects of the metabolic inhibitor carbonyl cyanide m-chlorophenylhydrazone have been examined at frog neuromuscular junctions. Carbonyl cyanide m-chlorophenylhydrazone (2 microM) caused a temperature-dependent block of evoked quantal transmitter release accompanied by an increase in the rate of spontaneous quantal release. The carbonyl cyanide m-chlorophenylhydrazone-induced increase in miniature endplate potential frequency was neither antagonized nor prevented by tetrodotoxin. It also occurred in a Ca2+-free medium and after replacement of Ca2+ by Sr2+, indicating that it does not depend upon a Na+ or Ca2+ influx from the external medium but may act by releasing Ca2+ from intraterminal stores. Spontaneous quantal transmitter release was exhausted irreversibly within 4 h of carbonyl cyanide m-chlorophenylhydrazone (2 microM) action, during which time an average of 4.7 x 10(5) acetylcholine quanta were released per junction. The morphologic analysis revealed a significant temperature and time-dependent reduction in the number of synaptic vesicles with swelling and dispersion of mitochondria within the motor nerve terminals. Changes in synaptic vesicle number appear to be directly related to the intensity of transmitter release. The good correlation observed between the number of quanta secreted and the number of vesicles lost by nerve terminals in the absence of vesicle recycling provides an estimate of the initial store of transmitter quanta.

摘要

在青蛙神经肌肉接头处,对量子化乙酰胆碱释放以及代谢抑制剂间氯苯腙羰基氰化物的超微结构效应进行了研究。间氯苯腙羰基氰化物(2微摩尔)引起了温度依赖性的诱发量子化递质释放阻滞,并伴有自发量子化释放速率的增加。间氯苯腙羰基氰化物诱导的微小终板电位频率增加既未被河豚毒素拮抗也未被其阻止。它也发生在无钙培养基中以及用Sr2+替代Ca2+之后,这表明它不依赖于来自外部介质的Na+或Ca2+内流,而是可能通过从终末内储存库释放Ca2+来发挥作用。在间氯苯腙羰基氰化物(2微摩尔)作用的4小时内,自发量子化递质释放不可逆地耗尽,在此期间每个接头平均释放4.7×105个乙酰胆碱量子。形态学分析显示,运动神经末梢内突触小泡数量显著减少,且线粒体肿胀和分散,这种减少具有温度和时间依赖性。突触小泡数量的变化似乎与递质释放的强度直接相关。在没有小泡循环的情况下,观察到分泌的量子数量与神经末梢丢失的小泡数量之间具有良好的相关性,这为递质量子的初始储存量提供了一个估计值。

相似文献

1
Effects of carbonyl cyanide m-chlorophenylhydrazone on quantal transmitter release and ultrastructure of frog motor nerve terminals.羰基氰化物间氯苯腙对蛙运动神经末梢量子递质释放及超微结构的影响
Neuroscience. 1988 Feb;24(2):695-708. doi: 10.1016/0306-4522(88)90362-4.
2
Sodium-dependent increase in quantal secretion induced by brevetoxin-3 in Ca2+-free medium is associated with depletion of synaptic vesicles and swelling of motor nerve terminals in situ.在无钙培养基中,短裸甲藻毒素-3诱导的依赖钠的量子分泌增加与突触小泡的耗竭和运动神经末梢原位肿胀有关。
Neuroscience. 1997 Jun;78(3):883-93. doi: 10.1016/s0306-4522(96)00568-4.
3
Ultrastructure of botulinum type-A poisoned frog motor nerve terminals after enhanced quantal transmitter release caused by carbonyl cyanide m-chlorophenylhydrazone.羰基氰化物间氯苯腙导致蛙运动神经终板量子递质释放增强后A型肉毒杆菌中毒的超微结构
Neurosci Lett. 1991 Sep 2;130(1):5-8. doi: 10.1016/0304-3940(91)90214-e.
4
Changes of quantal transmitter release caused by gadolinium ions at the frog neuromuscular junction.钆离子对青蛙神经肌肉接头处量子化递质释放的影响
Br J Pharmacol. 1991 Sep;104(1):133-8. doi: 10.1111/j.1476-5381.1991.tb12397.x.
5
Repetitive nerve stimulation decreases the acetylcholine content of quanta at the frog neuromuscular junction.重复神经刺激会降低青蛙神经肌肉接头处量子的乙酰胆碱含量。
J Physiol. 2001 May 1;532(Pt 3):637-47. doi: 10.1111/j.1469-7793.2001.0637e.x.
6
Reversible effect of depolarization by K-propionate on sub-miniature endplate potential to bell-miniature endplate potential ratios, on miniature endplate potential frequencies and amplitudes, and on synaptic vesicle diameters and densities in frog neuromuscular junctions.
Neuroscience. 1988 Dec;27(3):1055-72. doi: 10.1016/0306-4522(88)90210-2.
7
Caffeine and carbonyl cyanide m-chlorophenylhydrazone increased evoked and spontaneous release of luteinizing hormone-releasing hormone from intact presynaptic terminals.咖啡因和羰基氰化物间氯苯腙增加了来自完整突触前终末的促黄体生成素释放激素的诱发释放和自发释放。
Neuroscience. 1999;92(4):1511-21. doi: 10.1016/s0306-4522(99)00077-9.
8
Measurement of quantal secretion induced by ouabain and its correlation with depletion of synaptic vesicles.哇巴因诱导的量子分泌的测量及其与突触小泡耗竭的相关性。
J Cell Biol. 1985 Nov;101(5 Pt 1):1953-65. doi: 10.1083/jcb.101.5.1953.
9
Recycling and refilling of transmitter quanta at the frog neuromuscular junction.青蛙神经肌肉接头处递质量子的循环利用与再填充。
J Physiol. 2000 Feb 15;523 Pt 1(Pt 1):247-58. doi: 10.1111/j.1469-7793.2000.00247.x.
10
Correlation between quantal secretion and vesicle loss at the frog neuromuscular junction.青蛙神经肌肉接头处量子分泌与囊泡丢失之间的相关性。
J Physiol. 1990 Jun;425:501-26. doi: 10.1113/jphysiol.1990.sp018115.

引用本文的文献

1
Mitochondria at the neuronal presynapse in health and disease.线粒体在健康和疾病中的神经元突触前。
Nat Rev Neurosci. 2018 Jan 19;19(2):63-80. doi: 10.1038/nrn.2017.170.
2
Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals.线粒体对钙离子的摄取可防止量子释放的不同步,并在重复刺激小鼠运动神经末梢期间将耗竭降至最低。
J Physiol. 2003 Apr 15;548(Pt 2):425-38. doi: 10.1113/jphysiol.2002.035196. Epub 2003 Feb 14.
3
Effects of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one on synaptic vesicle cycling at the frog neuromuscular junction.
2-(4-吗啉基)-8-苯基-4H-1-苯并吡喃-4-酮对青蛙神经肌肉接头处突触小泡循环的影响。
J Neurosci. 2002 Dec 15;22(24):10680-9. doi: 10.1523/JNEUROSCI.22-24-10680.2002.
4
Repetitive nerve stimulation decreases the acetylcholine content of quanta at the frog neuromuscular junction.重复神经刺激会降低青蛙神经肌肉接头处量子的乙酰胆碱含量。
J Physiol. 2001 May 1;532(Pt 3):637-47. doi: 10.1111/j.1469-7793.2001.0637e.x.
5
Presynaptic function is altered in snake K+-depolarized motor nerve terminals containing compromised mitochondria.在含有受损线粒体的蛇K⁺去极化运动神经末梢中,突触前功能发生改变。
J Physiol. 2001 Apr 1;532(Pt 1):217-27. doi: 10.1111/j.1469-7793.2001.0217g.x.
6
Recycling and refilling of transmitter quanta at the frog neuromuscular junction.青蛙神经肌肉接头处递质量子的循环利用与再填充。
J Physiol. 2000 Feb 15;523 Pt 1(Pt 1):247-58. doi: 10.1111/j.1469-7793.2000.00247.x.
7
Effects of cadmium on quantal transmitter release and ultrastructure of frog motor nerve endings.镉对青蛙运动神经末梢量子递质释放及超微结构的影响。
J Neural Transm. 1989;77(2-3):79-91. doi: 10.1007/BF01248924.
8
Effects of charybdotoxin, a blocker of Ca2+-activated K+ channels, on motor nerve terminals.钙激活钾通道阻滞剂蝎毒素对运动神经末梢的影响。
Br J Pharmacol. 1988 Dec;95(4):1329-35. doi: 10.1111/j.1476-5381.1988.tb11772.x.