Negative cross‐talk between presynaptic adenosine and acetylcholine receptors
Negative cross‐talk between presynaptic adenosine and acetylcholine receptors
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突触前腺苷和乙酰胆碱受体之间的负串扰
DOI：
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发表时间：
2006
影响因子：
3.4
通讯作者：
R. Giniatullin
中科院分区：
文献类型：
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作者：
A. V. Shakirzyanova;E. Bukharaeva;E. Nikolsky;R. Giniatullin
通过记录沐浴或局部应用激动剂期间的微型终板电位（MEPP），研究了青蛙神经肌肉接头突触前腺苷和乙酰胆碱（ACh）自身受体之间的功能相互作用。腺苷作用于突触前腺苷 A1 受体 (EC50 = 1.1 μm) 或卡巴胆碱作用于毒蕈碱 M2 受体 (EC50 = 1.8 μm) 可以降低 MEPP 的频率。然而，当腺苷作用达到最大后使用卡巴胆碱时，并没有产生镇静作用。这种现象表明 A1 和 M2 受体之间发生了负串扰（遮挡）。此外，闭塞是受体特异性的，因为在腺苷存在的情况下应用 ATP 会继续降低 MEPP 频率。毒蕈碱拮抗剂[阿托品或1-[[2-[(二乙氨基)甲基)-1-哌啶基]乙酰基]-5,11-二氢-6H-吡啶并[2,3-b][1,4]苯二氮卓-6-酮)(AFDX-116)]对腺苷和的抑制作用没有影响 腺苷拮抗剂[8-(对磺苯基)茶碱(8-SPT)或1,3-二丙基-8-环戊基黄嘌呤(DPCPX)]对卡巴胆碱的作用没有影响。这些数据表明 A1 和 M2 受体之间没有发生膜界定的相互作用。卡巴胆碱和腺苷同样抑制高钾、离子霉素或蔗糖引发的量子释放。这些结果表明，M2 和 A1 受体激活的细胞内通路汇聚到位于 Ca2+ 流入下游的共同突触前效应器。我们认为，在强烈的突触活动期间，两个主要自身受体之间可能会发生负向串扰，从而减弱乙酰胆碱和腺苷的突触前抑制作用。
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 (EC50 = 1.1 µm) or by carbachol acting on muscarinic M2 receptors (EC50 = 1.8 µm). 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 Ca2+ 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.
选择性腺苷拮抗剂（8-环戊基-1,3-二丙基黄嘌呤）通过作用于 A1 受体消除神经肌肉抑制和外源腺苷的作用。
影响因子：
3.6
作者：
Redman,RS;Silinsky,EM
通讯作者：
Silinsky,EM
青蛙运动神经冲动发生后几毫秒内同步释放 ATP 和神经递质。
DOI：
10.1113/jphysiol.1996.sp021348
发表时间：
1996
期刊：
The Journal of physiology
影响因子：
--
作者：
Silinsky,EM;Redman,RS
通讯作者：
Redman,RS
大鼠神经肌肉传递过程中释放的腺苷来源。
DOI：
10.1113/jphysiol.1991.sp018388
发表时间：
1991
期刊：
The Journal of physiology
影响因子：
--
作者：
Smith,DO
通讯作者：
Smith,DO