Hilaire Cécile, Inquimbert Perrine, Al-Jumaily Mohammed, Greuet Denis, Valmier Jean, Scamps Frédérique
INSERM U 583, Hopital St. Eloi, 80, rue Augustin Fliche, BP 74103, 34091 Montpellier Cedex 5, France.
Neurosci Lett. 2005 Jun 3;380(3):330-4. doi: 10.1016/j.neulet.2005.01.068. Epub 2005 Feb 12.
Hyperexcitability of axotomized dorsal root ganglion neurons is thought to play a role in neuropathic pain. Numerous changes in ionic channels expression or current amplitude are reported after an axotomy, but to date no direct correlation between excitability of axotomized sensory neurons and ionic channels alteration has been provided. Following sciatic nerve injury, we examined, under whole-cell patch clamp recording, the effects of calcium homeostasis on the electrical activity of axotomized medium-sized sensory neurons isolated from lumbar dorsal root ganglia of adult mice. Axotomy induced an increase in excitability of medium sensory neurons among which 25% develop a propensity to fire repetitively. The condition necessary to get burst discharge in axotomized neurons was the presence of a high intracellular Ca2+ buffer concentration. The main effect was to amplify the increase in threshold current and apparent input resistance induced by axotomy. These data supply evidence for a role of Ca2+-dependent mechanisms in the control of excitability of axotomized sensory neurons.
轴突切断的背根神经节神经元的兴奋性过高被认为在神经性疼痛中起作用。轴突切断后,有许多关于离子通道表达或电流幅度变化的报道,但迄今为止,尚未发现轴突切断的感觉神经元兴奋性与离子通道改变之间存在直接关联。坐骨神经损伤后,我们在全细胞膜片钳记录下,研究了钙稳态对从成年小鼠腰段背根神经节分离出的轴突切断的中等大小感觉神经元电活动的影响。轴突切断导致中等大小感觉神经元的兴奋性增加,其中25%的神经元有重复放电的倾向。在轴突切断的神经元中产生爆发性放电的必要条件是细胞内高浓度的Ca2+缓冲剂。主要作用是放大轴突切断引起的阈电流增加和表观输入电阻增加。这些数据为Ca2+依赖机制在控制轴突切断的感觉神经元兴奋性中发挥作用提供了证据。