中文摘要：

目的：在大鼠颈上交感神经节（SCG）、结状神经节（NG）和耳副交感神经节（OTG）分离的神经元上，分别比较了Zn^2＋对P2X受体介导ATP诱导电流的调制作用。方法：用全细胞膜片钳技术观察Zn^2＋对以上3种大鼠自主神经节分离神经元ATP／αβ-me ATP诱导电流的调制作用。结果：在SCG的所有神经元上，ATP可以诱发一个缓慢型电流，同时给予Zn^2＋ （10μmol／L）可以使其反应增大至（1442±34）％，而αβ-me ATP没有此作用。在NG的所有神经元上，ATP和αβ-me ATP可以诱发一个类似的缓慢型电流，同时给予Zn^2＋可以使其反应分别增大至（180±12）％和（262±28）％。在OTG的所有神经元上，ATP可以诱发一个类似的缓慢型电流，同时给予Zn^2＋（10μmol／L），对ATP（10μmol／L）诱发的电流无明显影响；如果将ATP浓度提高至30μmol／L，同样浓度的Zn^2＋（10μmol／L）可以抑制ATP电流，而且随着Zn^2＋浓度的增高（10、100μmol／L），其抑制作用逐渐增强；如果先给予TNP—ATP（100nmol／L）阻断电流至未给予TNP—ATP组的（26±2）％，再给予Zn“（10t~mol／L）后，剩余的ATP电流为单独给予TNP—ATP的（127士9）％；αβ-me ATP也可以诱发一个类似的缓慢型电流，同时给予Zn^2＋（10μmol／L）可使其反应增大至（146±5）％；Zn^2＋（300μmol／L）对ATP和αβ—me ATP（30μmol／L）诱发电流的激活和失活时间常数均无明显影响。结论：（1）Zn^2＋对P2X受体具有变构性的调节作用，它可以增强大鼠SCG和NG上由P2X2和P2X2／3受体介导的缓慢型电流。（2）大鼠OTG上主要表达P2X2/3和少量P2X：受体，但Zn^2＋对ATP诱导的电流有轻度抑制作用，提示0TG可能存在着P2X受体家族的新亚型。

英文摘要：

Objective：To compare the effects of Zn^2＋ on the P2X receptor-mediated, ATP-induced currents in neurons separated from rat superior cervical ganglion （SCG）, nodose ganglion （NG）, and otic ganglion （OTG）. Methods.. Whole-cell patch clamp recording technique was used to study the regulatory effects of Zn2＋ on ATP/αβ-me ATP-induced currents in the above 3 ganlglion neurons. Results： All SCG neurons responded to ATP with a sustained current, while no neurons responded to αβ-me ATP：Zn^2＋ potentiated ATP-induced sustained currents to （1 442±34）% of the original value. All NG neurons responded to ATP and αβ-me ATP with a similar sustained current,coapplication of Zn^2＋ （10μmol/L） potentiated their responses to （180±12） % and （262±28）% ,respectively. All OTG neurons responded to both ATP and a~-me ATP with a sustained current. Coapplication of Zn^2＋ （10μmol/L） did not significantly potentiate the sustained currents induced by 10 μmol/L ATP, but when ATP was at 30μmol/L, Zn^2＋ （10-100μmol/L） inhibited ATP-induced sustained currents in a dose dependent manner. If TNP-ATP （100 nmol/L） was first used to inhibit ATP-induced current to （26±2）% of the original value, Zn^2＋ at 10μmol/L potentiated the inhibited current to （127±9）% of its original value. Coapplication of Zn^2＋ （10μmol/L） potentiated αβ-me ATP-induced currents to （146 5± 5）% of the control. Zn^2＋ （300μmol/L） had no effect on ton and toff of ATP- and αβ-me ATP-induced （30μmol/L） currents in OTG neurons. Conclusion, （1） Zn^2＋ is an allosteric modulator of P2X2 and P2X2/3 receptors in SCG and NG neurons and can potentiate the currents they induced. （2）The predominant receptor subtypes in OTG appear to be homomeric P2X2/3 and a little P2X2. Zn^2＋ has an inhibitory effect on the ATP-induced currents in OTG neurons, suggesting some novel members of the P2X purinoceptor exist in these neurons.