阈下膜电位振荡介导受损DRG神经元的交感敏化现象

Subthreshold membrane potential oscillation mediates adrenosensitivity in chronically compressed DRG neurons

目的 :在背根节 (dorsalrootganglion ,DRG)慢性压迫这一神经病理性痛模型研究交感敏化的膜机制 .方法 :采用离体细胞内记录 ,在受损DRG神经元观察去甲肾上腺素(norepinephrine,NE)对其膜电位的影响 .结果 :NE在受损(4 0 /45 )及正常 (1 5 /2 2 )DRG神经元均可以诱发膜电位的去极化过程 .NE诱发的膜电位去极化有浓度依赖性且可被酚妥拉明阻断 .仅有部分受损DRG神经元可在NE诱发的膜电位去极化基础上出现阈下膜电位振荡 (subthresholdmembranepotentialoscillation ,SMPO)并随后出现重复放电 .当应用TTX选择性地消除SMPO后 ,虽然NE诱发的膜电位去极化仍然存在 ,但神经元的重复放电不再产生 .结论 :触发及增大SMPO是NE诱发受损DRG神经元兴奋效应产生的一个关键因素 .

AIM: To investigate membrane mechanism of adrenosensitivity in a neuropathic pain model caused by chronic compression of dorsal root ganglion (DRG). METHODS: Effects of norepinephrine (NE, 10 μmol/L) on the membrane potential of DRG A neurons in rats were examined intracellularly in vitro . RESULTS: NE induced depolarization in both intact (15/22) and injured (40/45) DRG neurons. NE could induce membrane depolarization in a concentration dependent manner and could be blocked by phentolamine. Following NE induced depolarization, a subthreshold membrane potential oscillation (SMPO) could be triggered and enhanced, and consequently repetitive firing was initiated or increased only in some injured neurons (13/45). After SMPO was selectively abolished by tetrodotoxin (1 μmol/L), NE induced depolarization didn't produce repetitive firing again, even by a deep depolarization. CONCLUSION: These results strongly suggest that the triggering and enhancement of SMPO may be a critical step for mediating NE induced excitatory effects in the injured sensory neurons.