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腺苷可抑制神经递质释放,但并非大鼠神经肌肉接头处“强直后衰减”的原因。

Adenosine depresses transmitter release but is not the basis for 'tetanic fade' at the neuromuscular junction of the rat.

作者信息

Malinowski M N, Cannady S B, Schmit K V, Barr P M, Schrock J W, Wilson D F

机构信息

Department of Zoology, Center for Neuroscience, Miami University, Oxford, OH 45056, USA.

出版信息

Neurosci Lett. 1997 Jul 18;230(2):81-4. doi: 10.1016/s0304-3940(97)00480-1.

DOI:10.1016/s0304-3940(97)00480-1
PMID:9259469
Abstract

It has been suggested that during repetitive neural stimulation adenosine accumulates at the neuromuscular junction and the resulting negative feedback action of adenosine is the major basis for tetanic fade (decline in action of adenosine during repetitive stimulation) This hypothesis was examined at the rat neuromuscular junction by examining the effects of blocking adenosine A1-receptors. Intracellular recording techniques were used to monitor end-plate potentials and miniature end-plate potentials. The data suggest that while adenosine serves a role in depressing transmitter release, adenosine accumulation during brief periods of stimulation is minimal and adenosine is not the cause for tetanic fade.

摘要

有人提出,在重复神经刺激过程中,腺苷在神经肌肉接头处积累,而腺苷产生的负反馈作用是强直减退(重复刺激期间腺苷作用减弱)的主要基础。通过研究阻断腺苷A1受体的作用,在大鼠神经肌肉接头处对这一假说进行了检验。采用细胞内记录技术监测终板电位和微小终板电位。数据表明,虽然腺苷在抑制递质释放中起作用,但在短暂刺激期间腺苷的积累极少,且腺苷不是强直减退的原因。

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引用本文的文献

1
Tetanic depression is overcome by tonic adenosine A(2A) receptor facilitation of L-type Ca(2+) influx into rat motor nerve terminals.强直抑制可通过强直腺苷A(2A)受体促进L型Ca(2+)流入大鼠运动神经末梢来克服。
J Physiol. 2004 Oct 1;560(Pt 1):157-68. doi: 10.1113/jphysiol.2004.067595. Epub 2004 Aug 5.