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轴突-轴突耦合:一种超快速神经元通讯的新机制。

Axo-axonal coupling. a novel mechanism for ultrafast neuronal communication.

作者信息

Schmitz D, Schuchmann S, Fisahn A, Draguhn A, Buhl E H, Petrasch-Parwez E, Dermietzel R, Heinemann U, Traub R D

机构信息

Institute of Physiology, Charité, Humboldt-University Berlin, Tucholskystr. 2, 10117, Berlin, Germany.

出版信息

Neuron. 2001 Sep 13;31(5):831-40. doi: 10.1016/s0896-6273(01)00410-x.

Abstract

We provide physiological, pharmacological, and structural evidence that axons of hippocampal principal cells are electrically coupled, with prepotentials or spikelets forming the physiological substrate of electrical coupling as observed in cell somata. Antidromic activation of neighboring axons induced somatic spikelet potentials in neurons of CA3, CA1, and dentate gyrus areas of rat hippocampal slices. Somatic invasion by these spikelets was dependent on the activation of fast Na(+) channels in the postjunctional neuron. Antidromically elicited spikelets were suppressed by gap junction blockers and low intracellular pH. Paired axo-somatic and somato-dendritic recordings revealed that the coupling potentials appeared in the axon before invading the soma and the dendrite. Using confocal laser scanning microscopy we found that putative axons of principal cells were dye coupled. Our data thus suggest that hippocampal neurons are coupled by axo-axonal junctions, providing a novel mechanism for very fast electrical communication.

摘要

我们提供了生理学、药理学及结构学证据,表明海马体主细胞的轴突存在电耦合,预电位或小尖峰构成了电耦合的生理基础,这与在细胞体中观察到的情况一致。对相邻轴突的逆向激活在大鼠海马体切片的CA3、CA1和齿状回区域的神经元中诱发出体细胞小尖峰电位。这些小尖峰对体细胞的侵袭依赖于突触后神经元中快速钠通道的激活。逆向诱发的小尖峰被缝隙连接阻滞剂和低细胞内pH值所抑制。成对的轴突-体细胞和体细胞-树突记录显示,耦合电位在轴突侵入体细胞和树突之前就已出现。利用共聚焦激光扫描显微镜,我们发现主细胞的假定轴突存在染料耦合。因此,我们的数据表明,海马体神经元通过轴突-轴突连接实现耦合,为非常快速的电通信提供了一种新机制。

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