Suppr超能文献

蛋白激酶C对金鱼视网膜双极细胞递质释放的增强作用。

Potentiation of transmitter release by protein kinase C in goldfish retinal bipolar cells.

作者信息

Minami N, Berglund K, Sakaba T, Kohmoto H, Tachibana M

机构信息

Department of Psychology, Graduate School of Humanities and Sociology, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

出版信息

J Physiol. 1998 Oct 1;512 ( Pt 1)(Pt 1):219-25. doi: 10.1111/j.1469-7793.1998.219bf.x.

Abstract
  1. We examined whether transmitter release could be modified by the activation of protein kinase C (PKC) of retinal bipolar cells. A bipolar cell with a large axon terminal was isolated from the goldfish retina. The presynaptic Ca2+ current was measured under whole-cell voltage clamp, and the released transmitter (probably glutamate) was detected electrophysiologically by using the response of NMDA receptors of catfish horizontal cells as a reporter. 2. Transmitter release was potentiated by a PKC activator, phorbol 12-myristate 13-acetate (PMA), but not by an ineffective phorbol ester, 4alpha-phorbol 12,13-didecanoate. A PKC inhibitor, bisindolylmaleimide I, did not affect the transmitter release by itself but blocked the PMA-induced potentiation of transmitter release. These results suggest that the actions of PMA were mediated via the activation of PKC. 3. Introduction of 5 mM EGTA into the presynaptic terminals of bipolar cells revealed two separate components of transmitter release. A rapid component was triggered immediately after depolarization while a slow component appeared with a delay. Application of PMA selectively potentiated the slow component without affecting the Ca2+ dependence of exocytosis. 4. We suggest that the activation of PKC may modify the recruitment process of synaptic vesicles in retinal bipolar cells.
摘要
  1. 我们研究了视网膜双极细胞蛋白激酶C(PKC)的激活是否能改变神经递质的释放。从金鱼视网膜中分离出一个轴突终末较大的双极细胞。在全细胞膜片钳记录模式下测量突触前Ca2+电流,并以鲶鱼水平细胞NMDA受体的反应作为报告指标,通过电生理方法检测释放的神经递质(可能是谷氨酸)。2. 神经递质的释放可被PKC激活剂佛波酯12 -肉豆蔻酸13 -乙酸酯(PMA)增强,但不能被无效的佛波酯4α -佛波醇12,13 -十二烷酸酯增强。PKC抑制剂双吲哚马来酰亚胺I本身不影响神经递质的释放,但能阻断PMA诱导的神经递质释放增强。这些结果表明,PMA的作用是通过PKC的激活介导的。3. 向双极细胞的突触前终末内注入5 mM的乙二醇双乙醚四乙酸(EGTA),揭示了神经递质释放的两个独立成分。快速成分在去极化后立即触发,而慢速成分则有延迟出现。应用PMA选择性地增强了慢速成分,而不影响胞吐作用对Ca2+的依赖性。4. 我们认为PKC的激活可能会改变视网膜双极细胞中突触囊泡的募集过程。

相似文献

2
Regulation of transmitter release from retinal bipolar cells.视网膜双极细胞神经递质释放的调节。
Prog Biophys Mol Biol. 1999;72(2):109-33. doi: 10.1016/s0079-6107(99)00003-6.

引用本文的文献

7
The role of ribbons at sensory synapses.带状物在感觉突触中的作用。
Neuroscientist. 2009 Aug;15(4):380-91. doi: 10.1177/1073858408331373. Epub 2009 Mar 4.
9
Synaptic transmission at retinal ribbon synapses.视网膜带状突触处的突触传递。
Prog Retin Eye Res. 2005 Nov;24(6):682-720. doi: 10.1016/j.preteyeres.2005.04.002.

本文引用的文献

10

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验