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大鼠背根神经节神经元中刺突诱发的抑制和爆发模式

Spike-evoked suppression and burst patterning in dorsal root ganglion neurons of the rat.

作者信息

Amir R, Devor M

机构信息

Department of Cell and Animal Biology, Hebrew University of Jerusalem, Israel.

出版信息

J Physiol. 1997 May 15;501 ( Pt 1)(Pt 1):183-96. doi: 10.1111/j.1469-7793.1997.183bo.x.

Abstract
  1. A low level of spontaneous impulse discharge is generated within dorsal root ganglia (DRGs) in intact animals, and this activity is enhanced following nerve injury. Many physiological stimuli present in vivo are capable of augmenting this ectopic discharge. Whatever their cause, episodes of sharply accelerated DRG firing tend to be followed by 'after-suppression' during which discharge falls below baseline rate. In this study we examined the process of postexcitation suppression of firing rate, and how it shapes spike patterning in primary sensory neurons. 2. We recorded intracellularly from sensory neurons in excised rat DRGs in vitro. Trains of spikes triggered by intracellular current pulses evoked a prolonged hyperpolarizing shift. This shift appeared to be due to activation of a Ca(2+)-dependent K+ conductance (9K(Ca)). Spikes evoked by just-suprathreshold pulses triggered a hyperpolarizing shift and spike cessation. As the shift decayed, spiking was restored. The net result was bursty (on-off) discharge, a previously unexplained peculiarity of ectopic discharge in some DRG neurons in vivo. 3. Conditioning nerve tetani delivered to axons of neurons which share the DRG with the impaled neuron evoked transient depolarization ('cross-depolarization'). However, when stimulus strength was increased so as to include the axon of the impaled neuron, the net result was a hyperpolarizing shift. Nerve stimulation that straddled the threshold of the axon of the impaled neuron drove it intermittently, but it always drove axons of at least some neighbouring neurons. The result was dynamic modulation of the membrane potential of the impaled neuron as cross-depolarization and spike-evoked hyperpolarizing shifts played off against one another. Membrane potential shifted in the hyperpolarizing direction whenever the axon was activated, and shifted in the depolarizing direction whenever it was silent. Dynamic modulation of this sort probably also occurs in vivo when stimuli are drawn over the surface of the skin.
摘要
  1. 在完整动物的背根神经节(DRG)内会产生低水平的自发冲动发放,并且这种活动在神经损伤后会增强。体内存在的许多生理刺激都能够增强这种异位放电。无论其原因如何,DRG发放急剧加速的 episodes 之后往往会出现“后抑制”,在此期间放电率会降至基线水平以下。在本研究中,我们研究了放电率的兴奋后抑制过程,以及它如何塑造初级感觉神经元中的尖峰模式。2. 我们在体外从切除的大鼠DRG中的感觉神经元进行细胞内记录。细胞内电流脉冲触发的一系列尖峰诱发了长时间的超极化转变。这种转变似乎是由于Ca(2+)依赖性K+电导(9K(Ca))的激活。刚好高于阈值的脉冲诱发的尖峰触发了超极化转变和尖峰停止。随着转变衰减,尖峰发放恢复。最终结果是爆发性(开-关)放电,这是体内一些DRG神经元异位放电之前无法解释的特性。3. 向与被刺穿神经元共用DRG的神经元轴突施加条件性神经强直刺激会诱发短暂的去极化(“交叉去极化”)。然而,当刺激强度增加以包括被刺穿神经元的轴突时,最终结果是超极化转变。跨越被刺穿神经元轴突阈值的神经刺激间歇性地驱动它,但它总是驱动至少一些相邻神经元的轴突。结果是随着交叉去极化和尖峰诱发的超极化转变相互作用,被刺穿神经元的膜电位发生动态调制。每当轴突被激活时,膜电位就会向超极化方向移动,而每当它处于静息状态时,膜电位就会向去极化方向移动。当刺激在皮肤表面移动时,这种动态调制可能也会在体内发生。

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