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目的通过大鼠三叉神经节(TG)神经元体外培养及全细胞膜片钳技术,观察ATP对大鼠TG神经元上电压敏感性钾离子电流IA的调节及可能的机制。方法雄性SD大鼠TG神经元急性分离,体外培养4h后进行全细胞膜片钳记录。结果在TG神经元上ATP可以诱导三种型式的电流,即T型、S型和B型。ATP可以抑制T型神经元IA(P<0.05),这种作用可以被P2X3受体拮抗剂TNP-ATP拮抗,在S型神经元上ATP对IA无作用。在ATP未能诱导出内向电流的TG神经元,ATP仍然对IA有抑制作用,而且这一作用可以被P2Y受体的拮抗剂suramin拮抗。结论 ATP对分离培养的TG神经元上IA可以起到抑制作用,这一作用可能通过P2X3受体或P2Y受体来完成,但ATP对IA电流的作用机制目前尚不十分清楚。这一研究将为进一步阐明神经病理性痛的发生机制提供实验依据,为临床治疗提供理论基础。
OBJECTIVE: To investigate the regulation of ATP on the voltage-sensitive potassium current IA in rat TG neurons and its possible mechanism through in vitro culture of rat trigeminal ganglion (TG) neurons and whole-cell patch clamp technique. Methods The TG neurons were isolated from male Sprague-Dawley rats. Whole-cell patch-clamp recording was performed after cultured in vitro for 4 hours. Results ATP can induce three types of currents in TG neurons, namely T type, S type and B type. ATP inhibited T-type neurons IA (P <0.05), and this effect was antagonized by the P2X3 receptor antagonist TNP-ATP, which showed no effect on IA in S-type neurons. ATP still inhibits IA in TG neurons that ATP can not induce inward current, and this effect can be antagonized by suramin, an antagonist of the P2Y receptor. Conclusions ATP can inhibit IA in isolated and cultured TG neurons, which may be mediated by P2X3 receptor or P2Y receptor. However, the mechanism of action of ATP on IA current is not yet clear. This study will provide experimental evidence for further elucidating the mechanism of neuropathic pain and provide a theoretical basis for clinical treatment.