Xiong Z, Lu W, MacDonald J F
Department of Physiology, University of Toronto, Toronto, Canada M5S 1A8.
Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):7012-7. doi: 10.1073/pnas.94.13.7012.
Extracellular concentrations of Ca2+ change rapidly and transiently in the brain during excitatory synaptic activity. To test whether such changes in Ca2+ can play a signaling role we examined the effects of rapidly lowering Ca2+ on the excitability of acutely isolated CA1 and cultured hippocampal neurons. Reducing Ca2+ excited and depolarized neurons by activating a previously undescribed nonselective cation channel. This channel had a single-channel conductance of 36 pS, and its frequency of opening was inversely proportional to the concentration of Ca2+. The inhibition of gating of this channel was sensitive to ionic strength but independent of membrane potential. The ability of this channel to sense Ca2+ provides a novel mechanism whereby neurons can respond to alterations in the extracellular concentration of this key signaling ion.
在兴奋性突触活动期间,大脑中细胞外Ca2+浓度会迅速且短暂地发生变化。为了测试Ca2+的这种变化是否能发挥信号传导作用,我们研究了快速降低Ca2+对急性分离的CA1和培养的海马神经元兴奋性的影响。通过激活一种先前未描述的非选择性阳离子通道,降低Ca2+可使神经元兴奋并使其去极化。该通道的单通道电导为36 pS,其开放频率与Ca2+浓度成反比。该通道门控的抑制对离子强度敏感,但与膜电位无关。该通道感知Ca2+的能力提供了一种新机制,借此神经元能够对这种关键信号离子的细胞外浓度变化做出反应。