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少突胶质细胞对大鼠海马CA1区齿状回中轴突动作电位传导速度的调节作用。

Modulatory effects of oligodendrocytes on the conduction velocity of action potentials along axons in the alveus of the rat hippocampal CA1 region.

作者信息

Yamazaki Yoshihiko, Hozumi Yasukazu, Kaneko Kenya, Sugihara Toshimichi, Fujii Satoshi, Goto Kaoru, Kato Hiroshi

机构信息

Department of Neurophysiology, Yamagata University School of Medicine, 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan.

出版信息

Neuron Glia Biol. 2007 Nov;3(4):325-34. doi: 10.1017/S1740925X08000070.

Abstract

Like neurons and astrocytes, oligodendrocytes have a variety of neurotransmitter receptors and ion channels. However, except for facilitating the rapid conduction of action potentials by forming myelin and buffering extracellular K(+), little is known about the direct involvement of oligodendrocytes in neuronal activities. To investigate their physiological roles, we focused on oligodendrocytes in the alveus of the rat hippocampal CA1 region. These cells were found to respond to exogenously applied glutamate by depolarization through N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors. Electrical stimulation of the border between the alveus and stratum oriens evoked inward currents through several routes involving glutamate receptors and inward rectifier K(+) channels. Moreover, electrical stimulation resembling in vivo activity evoked long-lasting depolarization. To examine the modulatory effects of oligodendrocytes on neuronal activities, we performed dual, whole-cell recording on CA1 pyramidal neurons and oligodendrocytes. Direct depolarization of oligodendrocytes shortened the latencies of action potentials evoked by antidromic stimulation. These results indicate that oligodendrocytes increase the conduction velocity of action potentials by a mechanism additional to saltatory conduction, and that they have active roles in information processing in the brain.

摘要

与神经元和星形胶质细胞一样,少突胶质细胞也有多种神经递质受体和离子通道。然而,除了通过形成髓鞘和缓冲细胞外钾离子(K⁺)来促进动作电位的快速传导外,对于少突胶质细胞直接参与神经元活动的情况知之甚少。为了研究它们的生理作用,我们将重点放在大鼠海马CA1区的脑室下区的少突胶质细胞上。发现这些细胞通过N-甲基-D-天冬氨酸(NMDA)受体和非NMDA受体去极化,对外源性施加的谷氨酸作出反应。对脑室下区和原层之间的边界进行电刺激,通过涉及谷氨酸受体和内向整流钾离子(K⁺)通道的几种途径诱发内向电流。此外,类似于体内活动的电刺激诱发了持久的去极化。为了研究少突胶质细胞对神经元活动的调节作用,我们对CA1锥体神经元和少突胶质细胞进行了双细胞全细胞膜片钳记录。少突胶质细胞的直接去极化缩短了逆向刺激诱发动作电位的潜伏期。这些结果表明,少突胶质细胞通过跳跃传导以外的机制增加动作电位的传导速度,并且它们在大脑的信息处理中发挥着积极作用。

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