生物谷报道:肌肉收缩通常发生在神经递质分子从神经细胞释放到肌肉细胞的时候,然而来自美国犹他州大学的研究人员却发现裸露的次原子:质子能像大型的,复杂的神经递质一样导致微小圆蠕虫(线虫)内脏肌肉的收缩。这一研究成果今天公布在Cell(1月11日)杂志上。
领导这一研究的是生物学家Erik Jorgensen,犹他州大学大脑研究院科学主任。Jorgensen表示,“细胞内只有少数几种分子能作为神经递质启动电位变化,质子是将近20年以来这一家族的新成员。”
(图片来自Wayne Davis, University of Utah)
传统的神经递质,譬如serotonin, dopamine和GABA,都是由许多原子组成,这一新研究揭示了一个令人惊讶的发现:质子——失去电子的单个氢原子——能从一种圆蠕虫的内脏中通过某种蛋白释放出来,结合在邻近肌肉的受体蛋白上,导致肌肉收缩,从而引起蠕虫排便。
研究人员不仅发现质子能像神经递质一般工作,而且识别出了在蠕虫这一过程中的基因和蛋白,之前的研究表明人类和小鼠的大脑也具有能帮助质子在细胞间移动的质子泵(proton pumps,生物谷注)和受体,而这一新研究则进一步发现这些质子也许能作为大脑中的传递神经信号因子。
(图片上部为一正常线虫,下部为大便干燥的线虫,箭头指向线虫的内脏,图片来自Paola Nix, University of Utah)
另一研究员Wayne Davis表示,“这是第一次发现质子能作为神经递质”,“在人类可能也存在这些过程,人类和小鼠大脑和内脏细胞中有质子泵,其中一些被认为能帮助内脏消化食物,那么大脑中的质子泵用来干嘛呢?”
Jorgensen补充道,“缺乏质子受体的小鼠不具有学习能力,可能就是由于学习需要质子泵和受体的帮助。”
生物谷推荐原始出处:
Copyright © 2008 Cell Press. All rights reserved.
Cell, Vol 132, 149-160, 11 January 2008
Article
Protons Act as a Transmitter for Muscle Contraction in C. elegans
Asim A. Beg,1,2,3 Glen G. Ernstrom,2 Paola Nix,2 M. Wayne Davis,2 and Erik M. Jorgensen1,2,
1 Neuroscience Program, University of Utah, Salt Lake City, UT 84112-0840, USA
2 Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-0840, USA
Corresponding author
Erik M. Jorgensen
jorgensen@biology.utah.edu
Muscle contraction is normally mediated by the release of neurotransmitters from motor neurons. Here we demonstrate that protons can act as a direct transmitter from intestinal cells to stimulate muscle contraction. During the C. elegans defecation motor program the posterior body muscles contract even in the absence of neuronal inputs or vesicular neurotransmission. In this study, we demonstrate that the space between the intestine and the muscle is acidified just prior to muscle contraction and that the release of caged protons is sufficient to induce muscle contraction. PBO-4 is a putative Na+/H+ ion exchanger expressed on the basolateral membrane of the intestine, juxtaposed to the posterior body muscles. In pbo-4 mutants the extracellular space is not acidified and the muscles fail to contract. The pbo-5 and pbo-6 genes encode subunits of a “cys-loop” proton-gated cation channel required for muscles to respond to acidification. In heterologous expression assays the PBO receptor is half-maximally activated at a pH of 6.8. The identification of the mechanisms for release and reception of proton signals establishes a highly unusual mechanism for intercellular communication.