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首页> 外文期刊>The European Journal of Neuroscience >Modulation by adenosine of both muscarinic M1-facilitation and M2-inhibition of (3H)-acetylcholine release from the rat motor nerve terminals.
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Modulation by adenosine of both muscarinic M1-facilitation and M2-inhibition of (3H)-acetylcholine release from the rat motor nerve terminals.

机译：腺苷对毒蕈碱M1促进和M2抑制（3H）-乙酰胆碱从大鼠运动神经末梢释放的调节。

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摘要

The crosstalk between adenosine and muscarinic autoreceptors regulating evoked [3H]-acetylcholine ([3H]-ACh) release was investigated on rat phrenic nerve-hemidiaphragm preparations. Motor nerve terminals possess facilitatory M1 and inhibitory M2 autoreceptors that can be activated by McN-A-343 (1-30 microm) and oxotremorine (0.3-100 microm), respectively. The muscarinic receptor antagonist, dicyclomine (3 nm-10 microm), caused a biphasic (inhibitory/facilitatory) effect, indicating that M1-facilitation prevails during 5 Hz stimulation trains. Concomitant activation of AF-DX 116-sensitive M2 receptors was partially attenuated, as pretreatment with M1 antagonists, muscarinic toxin 7 (MT-7, 0.1 nm) and pirenzepine (1 nm), significantly enhanced inhibition by oxotremorine. Activation of A2A-adenosine receptors with CGS 21680C (2 nm) (i) potentiated oxotremorine inhibition, and (ii) shifted McN-A-343-induced facilitation into a small inhibitory effect. Conversely, the A1-receptor agonist, R-N6-phenylisopropyl adenosine (R-PIA, 100 nm), attenuated the inhibitory effect of oxotremorine, without changing facilitation by McN-A-343. Synergism between A2A and M2 receptors is regulated by a reciprocal interaction with facilitatory M1 receptors, which may be prevented by pirenzepine (1 nm). During 50 Hz-bursts, facilitation (M1) of [3H]-ACh release by McN-A-343 disappeared, while the inhibitory (M2) effect of oxotremorine became predominant. This muscarinic shift results from the interplay with A2A receptors, as it was precluded by the selective A2A receptor antagonist, ZM 241385 (10 nm). In conclusion, when the muscarinic M1 positive feedback loop is fully operative, negative regulation of ACh release is mediated by adenosine A1 receptors. During high frequency bursts, tonic activation of A2A receptors promotes M2 autoinhibition by braking the M1 receptor operated counteraction.
机译：在大鼠神经半ph制品上研究了腺苷与调节诱发的[3H]-乙酰胆碱（[3H] -ACh）释放的毒蕈碱自体受体之间的串扰。运动神经末梢具有促进性的M1和抑制性M2自身受体，可以分别由McN-A-343（1-30微米）和氧代短素（0.3-100微米）激活。毒蕈碱受体拮抗剂二环胺（3 nm-10微米）引起双相（抑制/促进）作用，表明在5 Hz刺激序列中普遍存在M1促进作用。 AF-DX 116敏感的M2受体的伴随激活被部分减弱，因为用M1拮抗剂，毒蕈碱毒素7（MT-7，0.1 nm）和哌仑西平（1 nm）预处理可以显着增强氧代雷莫林的抑制作用。用CGS 21680C（2 nm）激活A2A-腺苷受体（i）增强了氧代苯甲酸的抑制，并且（ii）将McN-A-343诱导的促进作用转变为小的抑制作用。相反，A1-受体激动剂R-N6-苯基异丙基腺苷（R-PIA，100 nm）减弱了氧代苯丁胺的抑制作用，而没有改变McN-A-343的促进作用。 A2A和M2受体之间的协同作用是通过与促进性M1受体的相互作用来调节的，哌仑西平（1 nm）可以阻止这种相互作用。在50 Hz的爆发过程中，McN-A-343释放[3H] -ACh的促进作用（M1）消失了，而氧代雷莫林的抑制作用（M2）成为主要作用。这种毒蕈碱迁移是由于与A2A受体的相互作用所致，因为选择性A2A受体拮抗剂ZM 241385（10 nm）阻止了这种变化。总之，当毒蕈碱M1阳性反馈环完全起作用时，腺苷A1受体介导ACh释放的负调节。在高频爆发期间，A2A受体的补品激活通过制动M1受体起作用的反作用而促进M2自抑制。

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