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慢性受压背根神经节神经元中异位自发放电的多个产生部位。

Multiple sites for generation of ectopic spontaneous activity in neurons of the chronically compressed dorsal root ganglion.

作者信息

Ma Chao, LaMotte Robert H

机构信息

Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.

出版信息

J Neurosci. 2007 Dec 19;27(51):14059-68. doi: 10.1523/JNEUROSCI.3699-07.2007.

Abstract

In a chronically compressed dorsal root ganglion (CCD) in the rat, a model of foraminal stenosis and radicular pain in human, a subpopulation of neurons with functional axons exhibits spontaneous activity (SA) that originates within the ganglion. Intracellular electrophysiological recordings were obtained from the somata of neurons of the compressed ganglion both in vitro and in vivo. The SA was classified into two types according to the presence (type I) or absence (type II) of subthreshold membrane potential oscillation. Neurons with type I SA had significantly higher somal excitability than those with type II SA. In most cases, depolarization of the membrane potential by current injection increased the discharge rates of type I--but not type II SA. Both types occasionally coexisted in the same neuron. Several lines of evidence suggested that the origin of SA in the DRG was most likely the soma for type I SA and the axon for type II. Therefore CCD neurons have multiple sites for generation of action potentials other than the terminal endings. In vivo recordings revealed the same two types of SA in a subpopulation of neurons with functionally characterized peripheral receptive fields. Thus, SA might not only produce spurious sensory input to the afferent pathways but also add to or block impulse transmission generated by natural stimulation of peripheral receptors. SA originating in the compressed ganglion is likely to interfere with sensory transmission in nociceptive and non-nociceptive neurons, thereby contributing to radicular pain, paresthesias, hyperalgesia and allodynia.

摘要

在大鼠慢性压迫性背根神经节(CCD)中,这是一种人类椎间孔狭窄和神经根性疼痛的模型,具有功能性轴突的神经元亚群表现出源于神经节内的自发活动(SA)。在体外和体内从受压神经节的神经元胞体获得细胞内电生理记录。根据阈下膜电位振荡的存在(I型)或不存在(II型),将SA分为两种类型。I型SA的神经元比II型SA的神经元具有显著更高的胞体兴奋性。在大多数情况下,通过电流注入使膜电位去极化会增加I型SA(而非II型SA)的放电率。两种类型偶尔会共存于同一神经元中。几条证据表明,DRG中SA的起源对于I型SA最可能是胞体,对于II型SA最可能是轴突。因此,CCD神经元除了终末之外还有多个产生动作电位的位点。体内记录显示,在具有功能特征性外周感受野的神经元亚群中存在相同的两种类型的SA。因此,SA不仅可能向传入通路产生虚假的感觉输入,还可能增强或阻断由外周感受器自然刺激产生的冲动传递。源于受压神经节的SA可能会干扰伤害性和非伤害性神经元中的感觉传递,从而导致神经根性疼痛、感觉异常、痛觉过敏和感觉异常性疼痛。

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