Lamotte D'Incamps B, Meunier C, Monnet M L, Jami L, Zytnicki D
URA CNRS 1448, Université René Descartes, Paris, France.
J Comput Neurosci. 1998 May;5(2):141-56. doi: 10.1023/a:1008861815083.
A compartmental model of myelinated nerve fiber was used to show that primary afferent depolarization (PAD), as elicited by axo-axonic synapses, reduces the amplitude of propagating action potentials primarily by interfering with ionic current responsible for the spike regeneration. This reduction adds to the effect of the synaptic shunt, increases with the PAD amplitude, and occurs at significant distances from the synaptic zone. PAD transiently enhances the sodium current activation, which partly accounts for the PAD-induced fiber hyperexcitability, and enhances sodium inactivation on a slower time course, thus reducing the amplitude of action potentials. In vivo, intraaxonal recordings from the intraspinal portion of group I afferent fibers were carried out to verify that depolarizations reduced the amplitude of propagating action potentials as predicted by the model. This article suggests PAD might play a major role in presynaptic inhibition.
一个有髓神经纤维的房室模型被用于表明，由轴-轴突触引发的初级传入去极化（PAD）主要通过干扰负责锋电位再生的离子电流来降低传播动作电位的幅度。这种降低叠加了突触分流的效应，随PAD幅度增加，并发生在距突触区相当远的距离处。PAD短暂增强钠电流激活，这部分解释了PAD诱导的纤维兴奋性增高，并且在较慢的时间进程中增强钠失活，从而降低动作电位的幅度。在体内，对I组传入纤维脊髓内部分进行轴内记录，以验证去极化是否如模型预测的那样降低传播动作电位的幅度。本文表明PAD可能在突触前抑制中起主要作用。
