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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Tuning adenosine A1 and A2A receptors activation mediates L-citrulline-induced inhibition of (3H)-acetylcholine release depending on nerve stimulation pattern.
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Tuning adenosine A1 and A2A receptors activation mediates L-citrulline-induced inhibition of (3H)-acetylcholine release depending on nerve stimulation pattern.

机译：调节腺苷A1和A2A受体的激活介导L-瓜氨酸诱导的（3H）-乙酰胆碱释放抑制，具体取决于神经刺激方式。

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摘要

The influence of nerve stimulation pattern on transmitter release inhibition by L-citrulline, the co-product of NO biosynthesis by nitric oxide synthase (NOS), was studied in the rat phrenic nerve-hemidiaphragm. We also investigated the putative interactions between NOS pathway and the adenosine system. L-citrulline (10-470 microM), the NOS substrate L-arginine (10-470 microM) and the NO donor 3-morpholinylsydnoneimine (SIN-1, 1-10 microM), concentration-dependently inhibited [(3)H]-acetylcholine ([(3)H]-ACh) release from rat motor nerve endings. Increasing stimulus frequency from 5 Hz-trains to 50 Hz-bursts enhanced [(3)H]-ACh release inhibition by l-arginine (47 microM) and L-citrulline (470 microM), whereas the effect of SIN-1 (10 microM) remained unchanged. NOS inhibition with N(omega)-nitro-L-arginine (100 microM) prevented the effect of L-arginine, but not that of L-citrulline. Adenosine deaminase (2.5 U/ml) and the adenosine transport inhibitor, S-(p-nitrobenzyl)-6-thioinosine (10 microM), attenuated release inhibition by L-arginine and L-citrulline. With 5 Hz-trains, blockade of A(1) receptors with 1,3-dipropyl-8-cyclopentyl xanthine (2.5 nM), but not of A(2A) receptors with ZM241385 (10nM), reduced the inhibitory action of l-arginine and L-citrulline; the opposite was verified with 50 Hz-bursts. Blockade of muscarinic M(2) autoreceptors with AF-DX116 (10 nM) also attenuated the effects of L-arginine and L-citrulline with 50 Hz-bursts. L-citrulline (470 microM) increased basal adenosine outflow via the equilibrative nucleoside transport system sensitive to NBTI (10 microM), without significantly (P>0.05) changing the nucleoside release subsequent to nerve stimulation. Data indicate that NOS-derived L-citrulline negatively modulates [(3)H]-ACh release by increasing adenosine outflow channelling to A(1) and A(2A) receptors activation depending on the stimulus paradigm. While adenosine acts predominantly at inhibitory A(1) receptors during 5 Hz-trains, inhibition of ACh release by L-citrulline at50 Hz-bursts depends on the interplay between adenosine A(2A) and muscarinic M(2) receptors.
机译：在大鼠stimulation神经半-中研究了神经刺激模式对一氧化氮合酶（NOS）合成NO的副产物L-瓜氨酸抑制递质释放的影响。我们还调查了NOS途径和腺苷系统之间的假定相互作用。 L-瓜氨酸（10-470 microM），NOS底物L-精氨酸（10-470 microM）和NO供体3-吗啉基亚磺酰亚胺（SIN-1，1-10 microM），浓度依赖性抑制[（3）H] -乙酰胆碱（[（3）H] -ACh）从大鼠运动神经末梢释放。刺激频率从5 Hz火车增加到50 Hz爆发，增强了L-精氨酸（47 microM）和L-瓜氨酸（470 microM）对[（3）H] -ACh释放的抑制，而SIN-1（10 microM）保持不变。用N（ω）-硝基-L-精氨酸（100 microM）抑制NOS阻止了L-精氨酸的作用，但没有阻止L-瓜氨酸的作用。腺苷脱氨酶（2.5 U / ml）和腺苷转运抑制剂S-（对硝基苄基）-6-硫代肌苷（10 microM），可减轻L-精氨酸和L-瓜氨酸的释放抑制。在5 Hz频率下，用1,3-二丙基-8-环戊基黄嘌呤（2.5 nM）阻断A（1）受体，但用ZM241385（10nM）阻断A（2A）受体，则降低了L-的抑制作用精氨酸和L-瓜氨酸;相反，用50 Hz突发进行了验证。与AF-DX116（10 nM）的毒蕈碱M（2）自受体的阻滞也减弱了L-精氨酸和L-瓜氨酸具有50 Hz猝发的作用。 L-瓜氨酸（470 microM）通过对NBTI敏感的平衡核苷转运系统（10 microM）增加了基础腺苷的流出，而在神经刺激后没有显着（P> 0.05）改变核苷的释放。数据表明，NOS衍生的L-瓜氨酸通过增加腺苷流出通道到A（1）和A（2A）受体的激活，取决于刺激范式，从而负调控[（3）H] -ACh的释放。虽然腺苷在5 Hz火车期间主要作用于抑制性A（1）受体，但L-瓜氨酸在50 Hz爆发时抑制ACh释放取决于腺苷A（2A）和毒蕈碱M（2）受体之间的相互作用。

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