摘要
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 observe the effect of ATP on transient outward potassium current (IA) and the underlying mechanism in the cultured trigeminal ganglion (TG) neurons by using whole-cell patch clamp technique. Methods The TG neurons were acutely separately from male SD rats and were cultured in vitro, and then were subjected to whole-cell patch clamp 4 h later. Results The results showed that the ATP-activated currents in rat TG neurons could be classified into three types (T, S and B type). ATP significantly inhibited IA on T type neurons (P^O. 05), and TNP-ATP, an antagonist of P2X3 receptors, could block the inhibitory effect of ATP against IA. ATP did not inhibit IA in S type neurons. Meanwhile, ATP could inhibit Ia in TG neurons in which ATP could not induce any inward currents. Suramin, an antagonist of P2Y receptors, could block the inhibitory effect of ATP against IA. Conclusion ATP can inhibit IAin cultured TG neurons, probably through P2X3 or P2Y receptors. Further studies are required to clarify the underlying mechanisms by which ATP affect Ia, which will cast lights on the mechanism of neuropathic pain and provide evidence for the clinical therapy.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2012年第7期712-717,共6页
Academic Journal of Second Military Medical University
基金
上海市科委基础重点项目(08JC1405400)~~