• 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

PKC-dependent reduction of the acetylcholine-evoked inward Na current in Aplysia D-neurons: effect of injected PKC and PKC activators.

作者信息

Papp A, Hoyer J

机构信息

Department of Neurophysiology, Max Planck Institute for Brain Research, Frankfurt, Germany.

出版信息

Brain Res. 1996 Feb 5;708(1-2):123-7. doi: 10.1016/0006-8993(95)01299-0.

DOI:10.1016/0006-8993(95)01299-0
PMID:8720867
Abstract

The effect of elevated PKC activity on the membrane depolarization (D-response) evoked by extracellular ACh, applied on the soma of Aplysia neurons, was studied. Intracellularly injected PKC and certain PKC activators were used to elevate PKC activity. ACh-induced current was measured in voltage clamp. The neurons were treated extracellularly with the PKC activators: PDAc, SC-10, R-59949, (-)-ILV; or with purified PKC injected into the neuron through the recording electrode. PKC injection and treatment with any of the PKC activators caused a similar reduction of the ACh-induced inward Na current response (corresponding to D-response), while the non-activating alpha-PDD had no effect. The results provide evidence that a PKC-dependent reduction of receptor responses also exists in this kind of Aplysia neurons. Furthermore, they show that the reduction of ACh response is indeed due to PKC activation (and not to a direct action of the phorbol ester).

摘要

相似文献

1
PKC-dependent reduction of the acetylcholine-evoked inward Na current in Aplysia D-neurons: effect of injected PKC and PKC activators.
Brain Res. 1996 Feb 5;708(1-2):123-7. doi: 10.1016/0006-8993(95)01299-0.
2
Presynaptic modification of synaptic transmission at identified Aplysia central synapses, induced by changes in protein kinase C activity.由蛋白激酶C活性变化诱导的,在已确定的海兔中枢突触处突触传递的突触前修饰。
Neurobiology (Bp). 1996;4(3):203-16.
3
Activators of protein kinase C mimic serotonin-induced modulation of a voltage-dependent potassium current in pleural sensory neurons of Aplysia.蛋白激酶C激活剂可模拟5-羟色胺对海兔胸膜感觉神经元中电压依赖性钾电流的调节作用。
J Neurophysiol. 1994 Sep;72(3):1240-9. doi: 10.1152/jn.1994.72.3.1240.
4
Alterations in the action potential of Aplysia neurons evoked by a phorbolester are mediated by protein kinase C.佛波酯诱发的海兔神经元动作电位的变化是由蛋白激酶C介导的。
Brain Res. 1995 Jun 26;684(1):107-11. doi: 10.1016/0006-8993(95)00437-u.
5
Modulation of IK,Ca by phorbol ester-mediated activation of PKC in pleural sensory neurons of Aplysia.佛波酯介导的蛋白激酶C激活对海兔胸膜感觉神经元中钙激活钾电流的调节作用
J Neurophysiol. 1992 Oct;68(4):1079-86. doi: 10.1152/jn.1992.68.4.1079.
6
Effects of protein kinase C activators and inhibitors on membrane properties, synaptic responses, and cholinergic actions in CA1 subfield of rat hippocampus in situ and in vitro.蛋白激酶C激活剂和抑制剂对大鼠海马CA1亚区原位和体外膜特性、突触反应及胆碱能作用的影响。
Synapse. 1991 Mar;7(3):193-206. doi: 10.1002/syn.890070304.
7
Differential effects of 4-aminopyridine, serotonin, and phorbol esters on facilitation of sensorimotor connections in Aplysia.4-氨基吡啶、血清素和佛波酯对海兔感觉运动连接易化作用的差异效应。
J Neurophysiol. 1997 Jan;77(1):177-85. doi: 10.1152/jn.1997.77.1.177.
8
Protein kinase C activation in Aplysia neurons by phorbol diacetate: comparison of effects following extracellular or intracellular application.佛波酯对海兔神经元蛋白激酶C的激活作用:细胞外或细胞内应用后的效果比较
Acta Physiol Hung. 1993;81(2):147-57.
9
Effect of HgCl2 on acetylcholine, carbachol, and glutamate currents of Aplysia neurons.氯化汞对海兔神经元乙酰胆碱、卡巴胆碱和谷氨酸电流的影响。
Cell Mol Neurobiol. 1994 Dec;14(6):653-64. doi: 10.1007/BF02088674.
10
cis-Fatty acids, which activate protein kinase C, attenuate Na+ and Ca2+ currents in mouse neuroblastoma cells.顺式脂肪酸可激活蛋白激酶C,减弱小鼠神经母细胞瘤细胞中的钠离子和钙离子电流。
J Physiol. 1989 Dec;419:95-119. doi: 10.1113/jphysiol.1989.sp017863.