摘要
目的:研究坐骨神经损伤后,大鼠背根神经节(dorsal root ganglion,DRG)C类初级感觉神经元膜表面唾液酸含量变化对其电生理特性的影响。方法:制作大鼠慢性压迫性神经损伤(chronic constriction injury,CCI)痛觉模型,以正常大鼠为对照,采用胞内电生理记录法检测损伤及正常C类神经元的电生理特性,随后用Ca^(2+)去中和损伤及正常C类神经元膜表面唾液酸所带负电荷或用唾液酸酶(neuraminidase,NA)分解膜表面唾液酸,观察电生理特性的变化。结果:损伤性C类神经元的静息电位(rest potential,RP)较正常C类神经元移向去极化方向,诱发动作电位(action potential,AP)发生率增加,所需阈强度减小,兴奋性增加;使用Ca^(2+)和唾液酸酶使损伤性C类神经元膜电位向超极化方向移动,诱发AP所需阈强度增加,兴奋性降低。而Ca^(2+)和唾液酸酶对正常C类神经元的电生理特性及兴奋性无影响。结论:损伤C类神经元膜表面唾液酸含量增加,导致其RP去极化且兴奋性增加。
AIM： To study the change of electrophysiological property of dorsal root ganglion（ DRG） C-type primary sensory neurons with sialic acid on the membrane surface after rat sciatic nerve injury. METHODS： The operation to induce chronic constriction nerve injury（ CCI） for establishing CCI pain model was performed in the rats,and normal rats served as controls. The thermal hyperalgesia behavior was observed to select CCI pain rats,and electrophysiological property of injured and normal C-type neurons was studied by intracellular recording. Ca^（2＋）and neuraminidase（ NA） were topically added on the extracellular membrane of C-type neurons to counteract or selectively remove the negatively charged sialic acid residues,and at the same time the change of electrophysiological property was observed. RESULTS： The rest potential（ RP） of injured C-type neurons shifted to depolarizing direction. The incidence of evoked action potential（ AP）was higher,and the rheobase to evoke AP was lower than the control. After topical application of Ca^（2＋）and NA on injured C-type neurons,hyperpolarized RP and increased rheobase to evoke AP were observed,indicating the excitability of injured C-type neurons diminished. However,these treatments to normal neurons had no effect on electrophysiological property.CONCLUSION： Increased negative charge on the injured C-type neuron surface,carried by the sialic acid residues,contributes to the change of electrophysiological property.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2016年第5期943-946,共4页
Chinese Journal of Pathophysiology
基金
山西省自然科学基金资助项目(No.2012011042-3)
