Suppression of nicotinic synaptic transmission by adenosine in myenteric ganglia of the guinea-pig gastric antrum.
Suppression of nicotinic synaptic transmission by adenosine in myenteric ganglia of the guinea-pig gastric antrum.
复制标题
腺苷在豚鼠胃窦肌间神经节中抑制烟碱突触传递。
DOI：
10.1016/0014-2999(92)90203-g
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发表时间：
1992
影响因子：
5
通讯作者：
Wood,JD
中科院分区：
文献类型：
--
作者：
Christofi,FL;Tack,J;Wood,JD
应用细胞内记录技术研究了腺苷对胃窦肌间神经元烟碱胆碱能传递的作用。腺苷或其更强的衍生物5′-N-乙基甲酰氨基腺苷（NECA）、5′-N-环丙基甲酰氨基腺苷、1-脱氮-2-氯-N6-环戊基腺苷或N6-环戊基腺苷可逆地抑制60%的胃神经元的快兴奋性突触后电位（fast excitatory postsynaptic potentials，fast EPSP），并呈剂量依赖性。腺苷和NECA均不影响对烟碱激动剂1，1-二甲基-4-苯基哌嗪碘的兴奋性反应。腺苷抑制快兴奋性突触后电位（EPSP）的EC 50浓度为55 μM，NECA是比腺苷更有效的抑制剂。特异性腺苷受体拮抗剂1，3-二丙基-8-对磺苯基黄嘌呤或1，3-二丙基-8-（环戊基）黄嘌呤可阻断腺苷或NECA的抑制作用。快速EPSP增强灌流的拮抗剂单独，提示内源性腺苷的烟碱传输的持续抑制。拮抗剂对静息膜特性、兴奋性或逆向动作电位没有影响。在具有快速EPSP抑制的神经元中，腺苷并不抑制对同一神经元的所有胆碱能输入。结果表明，腺苷抑制烟碱传递与突触前P1腺苷受体位于胆碱能释放网站。
Conventional intracellular recording techniques were used to investigate actions of adenosine on nicotinic cholinergic transmission in myenteric neurons of the gastric antrum. Adenosine or the more potent derivatives, 5′-N-ethylcarboxamidoadenosine (NECA), 5′-N-cyclopropylcarboxamidoadenosine, 1-deaza-2-chloro-N6-cyclopentyladenosine or N6-cyclopentyladenosine reversibly and dose dependently inhibited the fast excitatory postsynaptic potentials (fast EPSPs) in 60% of the gastric neurons. Neither adenosine nor NECA affected excitatory responses to the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium iodine. The EC50concentration for inhibition of the fast excitatory postsynaptic potential (EPSP) by adenosine was 55 μM NECA was a more potent inhibitor than adenosine. The specific adenosine receptor antagonists 1,3-dipropyl-8-p-sulfophenyl xanthine or 1,3-dipropyl-8-(cyclopentyl) xanthine blocked the inhibitory effects of adenosine or NECA. Fast EPSPs were enhanced by superfusion of the antagonists alone, suggestive of ongoing inhibition of nicotinic transmission by endogenous adenosine. The antagonists had no effect on resting membrane properties, excitability or antidromic action potentials. In neurons with suppression of fast EPSPs, adenosine did not suppress all cholinergic inputs to the same neuron. The results suggest that adenosine inhibits nicotinic transmission by interacting with presynaptic P1adenosine receptors located at cholinergic release sites.