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首页> 外文期刊>The European Journal of Neuroscience >Distinct receptors and different transduction mechanisms for ATP and adenosine at the frog motor nerve endings.
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Distinct receptors and different transduction mechanisms for ATP and adenosine at the frog motor nerve endings.

机译：青蛙运动神经末梢的ATP和腺苷的不同受体和不同的转导机制。

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Corelease of ATP with ACh from motor endings suggests a physiological role for ATP in synaptic transmission. We previously showed that, on skeletal muscle, ATP directly inhibited ACh release via presynaptic P2 receptors. The receptor identification (P2X or P2Y) and its transduction mechanism remained, however, unknown. In the present study using the voltage-clamp technique we analyzed the properties of presynaptic ATP receptors and subsequent effector mechanisms. ATP or adenosine presynaptically depressed multiquantal end-plate currents, with longer latency for ATP action. ATPgammaS, agonist at P2X receptors, or Bz-ATP, agonist at P2X7 receptors, were ineffective. The action of ATP was prevented by suramin and unchanged by PPADS or TNP-ATP, antagonists of P2X receptors, or RB-2, a blocker of certain P2Y receptors. The depressant action of ATP was reproduced by UTP, metabotropic P2Y receptor agonist. Pertussis toxin (PTX), antagonist of Gi/o-proteins, and inhibitors of phosphatidylcholine specific PLC (D609) and PKC (staurosporine or chelerythrine) prevented the effect of ATP while blockers of PLA2 (OBAA) and COX (aspirin or indomethacin) attenuated it. Inhibitors of phosphatidylinositide-specific PLC (U73122), guanylylcyclase (ODQ), PKA (Rp-cAMPS) or PLD (1-butanol) did not affect the action of ATP. No inhibitor of second messengers (except PTX) changed the action of adenosine. Our data indicate, for motor nerve endings, the existence of inhibitory P2Y receptors coupled to multiple intracellular cascades including phosphatidylinositide-specific PLC/PKC/PLA2/COX. This divergent presynaptic P2 signalling (unlike the single effector mechanism for P1 receptors) could provide feedback inhibition of transmitter release and perhaps be involved in presynaptic plasticity.
机译：ATP与ACh从运动末端共释放提示ATP在突触传递中具有生理作用。我们先前显示，在骨骼肌上，ATP通过突触前P2受体直接抑制ACh释放。受体识别（P2X或P2Y）及其转导机制仍然未知。在本研究中使用电压钳技术，我们分析了突触前ATP受体的性质和随后的效应器机制。 ATP或腺苷突触抑制多量子终板电流，ATP作用的潜伏期更长。 P2X受体激动剂ATPgammaS或P2X7受体激动剂Bz-ATP无效。苏拉明阻止了ATP的作用，而PPADS或TNP-ATP（P2X受体的拮抗剂）或RB-2（某些P2Y受体的阻滞剂）阻止了ATP的作用。 ATP的抑制作用由代谢型P2Y受体激动剂UTP再现。百日咳毒素（PTX），Gi / o蛋白的拮抗剂以及磷脂酰胆碱特异性PLC（D609）和PKC（星形孢菌素或白屈菜红碱）的抑制剂可阻止ATP的作用，而PLA2（OBAA）和COX（阿司匹林或消炎痛）的阻滞剂减弱它。磷脂酰肌醇特异性PLC（U73122），鸟苷酸环化酶（ODQ），PKA（Rp-cAMPS）或PLD（1-丁醇）的抑制剂不影响ATP的作用。第二信使的抑制剂（PTX除外）没有改变腺苷的作用。我们的数据表明，对于运动神经末梢，抑制性P2Y受体的存在与多个细胞内级联反应相关，包括磷脂酰肌醇特异性PLC / PKC / PLA2 / COX。这种不同的突触前P2信号传导（不同于P1受体的单一效应器机制）可能提供递质释放的反馈抑制作用，并且可能参与突触前的可塑性。

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