关节炎大鼠背根神经节细胞的膜电生理学特征

目的:研究炎症大鼠背根神经节(dorsal root ganglion,DRG)细胞的膜电生理学特征,试图解释炎症痛敏的机制.方法:应用全细胞膜片箝电流箝制技术,对急性分离的大鼠DRG细胞进行电流箝制.以完全弗氏佐剂诱发大鼠关节炎,分别取炎症痛急性期(24～72 h)和慢性期(2～3周)大鼠腰5、腰6 DRG细胞进行研究.结果:炎症痛急性期小型DRG细胞与对照组比动作电位的阈值增加8%(P＜0.01),小型及中型DRG细胞的动作电位的时程加宽75%和68%(P＜0.01),小细胞的细胞膜固有电阻增加25%(P＜0.05);炎症痛慢性期大鼠小DRG细胞动作电位的阈值增加(7%,P＜0.01),时程增加23%(P＜0.01),固有电阻下降24%(P＜0.01),而中型DRG细胞膜电特性无显著变化.结论:DRG细胞动作电位的时程加宽,促进了伤害性信息引起DRG细胞突触前膜Ca2+内流介导的递质释放,这可能是引发动物炎症痛敏的主要原因.

The electrophysiological characters of dorsal root ganglion neurons obtained from arthritic rats

Objective: To better understand the peripheral mechanism of inflammatory pain. Methods: The isolated neurons of dorsal root ganglion (DRG) were studied using the whole cell patch clamp technique in current clamp mode. DRG neurons were obtained from rats with arthritis induced by complete Freund's adjuvant (CFA). Results: The cell body of DRG in acute inflammation phase showed an increase 8% ( P <0.01) of the threshold values of action potential (AP), a widening of the action potential duration (APD) of small and median DRG cells (75% and 68%, P <0.01), and a 25% increase of the specific resistance (Rs) of small DRG cells ( P <0.05). In chronic inflammatory period, there was a 7% increase of the threshold value of AP ( P <0.01), a 23% widening of the APD ( P <0.01), and a 24% decrease of the Rs ( P <0.01). Conclusion: The widening of APD will strengthen the release of neurotransmitters from the small DRG neuron nerve terminal induced by unit afferent impulse, and it may serve as the main factor contributing to inflammatory hyperalgesia.