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首页> 外文期刊>The European Journal of Neuroscience >Negative cross-talk between presynaptic adenosine and acetylcholine receptors.
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Negative cross-talk between presynaptic adenosine and acetylcholine receptors.

机译：突触前腺苷和乙酰胆碱受体之间的负串扰。

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Functional interactions between presynaptic adenosine and acetylcholine (ACh) autoreceptors were studied at the frog neuromuscular junction by recording miniature end-plate potentials (MEPPs) during bath or local application of agonists. The frequency of MEPPs was reduced by adenosine acting on presynaptic adenosine A1 receptors (EC(50) = 1.1 microm) or by carbachol acting on muscarinic M2 receptors (EC(50) = 1.8 microm). However, carbachol did not produce the depressant effect when it was applied after the action of adenosine had reached its maximum. This phenomenon implied that the negative cross-talk (occlusion) had occurred between A1 and M2 receptors. Moreover, the occlusion was receptor-specific as ATP applied in the presence of adenosine continued to depress MEPP frequency. Muscarinic antagonists [atropine or 1-[[2-[(diethylamino)methyl)-1-piperidinyl]acetyl]-5,11-dihydro-6H-pyrido [2,3-b][1,4]benzodiazepine-6-one) (AFDX-116)] had no effect on the inhibitory action of adenosine and adenosine antagonists [8-(p-sulfophenyl)theophylline (8-SPT) or 1,3-dipropyl-8-cyclopentylxanthine (DPCPX)] had no effect on the action of carbachol. These data suggested that membrane-delimited interactions did not occur between A1 and M2 receptors. Both carbachol and adenosine similarly inhibited quantal release triggered by high potassium, ionomycin or sucrose. These results indicated a convergence of intracellular pathways activated by M2 and A1 receptors to a common presynaptic effector located downstream of Ca(2+) influx. We propose that the negative cross-talk between two major autoreceptors could take place during intense synaptic activity and thereby attenuate the presynaptic inhibitory effects of ACh and adenosine.
机译：通过在沐浴或局部应用激动剂时记录微型终板电位（MEPP），在青蛙神经肌肉连接处研究突触前腺苷和乙酰胆碱（ACh）自体受体之间的功能相互作用。腺苷作用于突触前腺苷A1受体（EC（50）= 1.1微米）或卡巴胆碱作用于毒蕈碱M2受体（EC（50）= 1.8微米），从而降低了MEPPs的频率。但是，在腺苷作用达到最大后，再施用卡巴胆碱并不会产生抑制作用。此现象暗示在A1和M2受体之间发生了负串扰（阻塞）。此外，闭塞是受体特异性的，因为在存在腺苷的情况下施加的ATP继续抑制MEPP频率。毒蕈碱拮抗剂[阿托品或1-[[[[2-[（（二乙基氨基）甲基）-1-哌啶基]乙酰基] -5,11-二氢-6H-吡啶基[2,3-b] [1,4]苯并二氮杂-6- 1）（AFDX-116）]对腺苷和腺苷拮抗剂[8-（对-磺基苯基）茶碱（8-SPT）或1,3-二丙基-8-环戊基黄嘌呤（DPCPX）]的抑制作用没有影响对卡巴胆碱作用的影响。这些数据表明膜分隔的相互作用在A1和M2受体之间没有发生。卡巴胆碱和腺苷均相似地抑制高钾，离子霉素或蔗糖引发的定量释放。这些结果表明由M2和A1受体激活的细胞内通路向位于Ca（2+）流入下游的常见突触前效应物的收敛。我们建议在强烈的突触活动期间，两个主要的自体受体之间可能发生负串扰，从而减弱ACh和腺苷对突触前的抑制作用。

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