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Zn2+对大鼠不同自主神经节分离神经元P2X受体介导ATP诱导电流的调制作用
马蓓,倪鑫,MABei,NIXin
0
()
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Zn2+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Zn2+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Zn2+(10μmol/L)可以使其反应增大至(1 442±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Zn2+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Zn2+(10 μmol/L),对ATP(10 μmol/L)诱发的电流无明显影响;如果将ATP浓度提高至30 μmol/L,同样浓度的Zn2+(10μmol/L)可以抑制ATP电流,而且随着Zn2+浓度的增高(10、100 μmol/L),其抑制作用逐渐增强;如果先给予TNP-ATP(100 nmol/L)阻断电流至未给予TNP-ATP组的(26±2)%,再给予Zn2+(10μmol/L)后,剩余的ATP电流为单独给予TNP ATP的(127±9)%;αβ-me ATP也可以诱发一个类似的缓慢型电流,同时给予Zn2+(10 μmol/L)可使其反应增大至(146±5)%;Zn2+(300μmol/L)对ATP和αβme ATP(30 μmol/L)诱发电流的激活和失活时间常数均无明显影响.结论:(1)Zn2+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P2X2受体,但Zn2+对ATP诱导的电流有轻度抑制作用,提示OTG可能存在着P2X受体家族的新亚型.
关键词:  Zn2+、神经节,自主、神经元、P2X受体、ATP诱导电流
DOI:10.3724/SP.J.1008.2006.00373
基金项目:国家自然科学基金(30570597).
Regulatory effect of Zn2+ on P2X receptor-mediated,ATP-induced currents in different autonomic ganglion neurons in rats
马蓓,倪鑫,MA Bei,NI Xin
()
Abstract:
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.
Key words:  Zn^2+  ganglia, autonomic  neurons  P2X receptors  ATP-induced currents