Darbon Pascal, Pignier Christophe, Niggli Ernst, Streit Jürg
Departement of Physiology, University of Bern, CH-3012 Bern, Switzerland.
J Neurophysiol. 2002 Sep;88(3):1461-8. doi: 10.1152/jn.2002.88.3.1461.
Disinhibition of rat spinal networks induces a spontaneous rhythmic bursting activity. The major mechanisms involved in the generation of such a bursting are intrinsic neuronal firing of a subpopulation of interneurons, recruitment of the network by recurrent excitation, and autoregulation of neuronal excitability. We have combined whole cell recording with calcium imaging and flash photolysis of caged-calcium to investigate the contribution of Ca(2+) to rhythmogenesis. We found that calcium mainly enters the neurons through voltage-activated calcium channels and N-methyl-D-aspartate (NMDA) channels as a consequence of the depolarization during the bursts. However, Ca(2+) could neither predict the start nor the termination of bursts and is therefore not critically involved in rhythmogenesis. Also calcium-induced calcium release is not involved as a primary mechanism in bursting activity. From these findings, we conclude that in the rhythmic activity induced by disinhibition of spinal cord networks, the loading of the cells with calcium is a consequence of bursting and does not functionally contribute to rhythm generation.
大鼠脊髓网络的去抑制会诱导出自发性节律性爆发活动。产生这种爆发的主要机制包括中间神经元亚群的内在神经元放电、通过反复兴奋对网络的募集以及神经元兴奋性的自动调节。我们将全细胞记录与钙成像以及笼锁钙的闪光光解相结合，以研究细胞内钙离子浓度（Ca(2+)）对节律发生的作用。我们发现，在爆发期间由于去极化，钙主要通过电压门控钙通道和N-甲基-D-天冬氨酸（NMDA）通道进入神经元。然而，Ca(2+)既不能预测爆发的开始也不能预测其终止，因此在节律发生中并非关键因素。此外，钙诱导的钙释放也不是爆发活动的主要机制。基于这些发现，我们得出结论，在脊髓网络去抑制诱导的节律性活动中，细胞内钙的负载是爆发的结果，在功能上对节律产生没有贡献。
