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Synaptic control of motoneuronal excitability.
Physiological Reviews ( IF 29.9 ) Pub Date : 2000-04-01 , DOI: 10.1152/physrev.2000.80.2.767
J C Rekling 1 , G D Funk , D A Bayliss , X W Dong , J L Feldman
Affiliation  

Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre- and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre- and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K(+) current, cationic inward current, hyperpolarization-activated inward current, Ca(2+) channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

中文翻译:

运动神经元兴奋性的突触控制。

运动是行为的基本组成部分,也是大脑的主要外在作用,是当骨骼肌响应运动神经元产生的动作电位模式而收缩和放松时产生的。因此,决定运动神经元放电行为的过程对于理解神经活动向运动行为的转变非常重要。在这里,我们回顾了最近关于运动神经元兴奋性控制的研究,重点关注突触和细胞特性。我们首先介绍运动神经元的背景描述:它们的发育、解剖组织以及被动和主动的膜特性。然后,我们描述运动神经元突触输入的一般解剖结构,然后描述影响运动神经元兴奋性的主要递质系统,包括配体、受体分布、突触前和突触后作用、信号转导和功能作用。谷氨酸是主要的兴奋性递质,GABA 和甘氨酸是通过离子型受体发挥作用的主要抑制性递质。这些氨基酸发出来自外周、脊柱和脊柱上结构的主要运动命令的信号。胺类,如血清素和去甲肾上腺素,神经肽,以及作用于代谢受体的谷氨酸和 GABA,通过突触前和突触后作用调节运动神经元的兴奋性。主要通过第二信使系统起作用,它们的作用集中在共同的效应器上,例如漏K(+)电流、阳离子内向电流、超极化激活的内向电流、Ca(2+)通道或突触前释放过程。这些众多的输入共同调节和修改传入的运动命令,最终生成协调的发射模式,该模式是运动行为期间肌肉收缩的基础。
更新日期:2019-11-01
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