Multiple sites for generation of ectopic spontaneous activity in neurons of the chronically compressed dorsal root ganglion
Multiple sites for generation of ectopic spontaneous activity in neurons of the chronically compressed dorsal root ganglion
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DOI：
10.1523/jneurosci.3699-07.2007
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发表时间：
2007-12-19
影响因子：
5.3
通讯作者：
LaMotte, Robert H.
中科院分区：
文献类型：
--
作者：
Ma, Chao;LaMotte, Robert H.
在慢性压迫的大鼠背根神经节（CCD）中，一种人的椎间孔狭窄和根性疼痛的模型，具有功能性轴突的神经元亚群表现出起源于神经节内的自发活动（SA）。在体和离体条件下，对受压神经节神经元胞体进行了细胞内电生理记录。根据阈下膜电位振荡的存在与否，将SA分为两种类型。与I型SA的神经元有显着较高的体兴奋性比那些与II型SA。在大多数情况下，通过电流注入的膜电位的去极化增加了I型SA的放电率，但不是II型SA。这两种类型偶尔共存于同一个神经元。几条证据表明，SA在DRG中的起源最有可能是索马的I型SA和轴突的II型。因此，CCD神经元具有多个产生动作电位的位点，而不是末端。在体内记录揭示了相同的两种类型的SA在一个亚群的神经元的功能特征的外周感受野。因此，SA不仅可能产生虚假的感觉输入到传入通路，但也增加或阻止由外周受体的自然刺激产生的脉冲传输。源自受压神经节的SA可能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、痛觉过敏和异常性疼痛。
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.