Center of Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Center of Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria
Am J Physiol Cell Physiol. 2014 Jun 15;306(12):C1200-13. doi: 10.1152/ajpcell.00329.2013. Epub 2014 Apr 23.
In the central nervous system, L-type voltage-gated calcium channels (LTCCs) come in two isoforms, namely Cav1.2 and Cav1.3 channels. It has been shown previously that these channels differ in biophysical properties, in subcellular localization, and in the coupling to the gene transcription machinery. In previous work on rat hippocampal neurons we have identified an excitatory cation conductance and an inhibitory potassium conductance as important LTCC coupling partners. Notably, a stimulus-dependent interplay of LTCC-mediated Ca(2+) influx and activation of these Ca(2+)-dependent conductances was found to give rise to characteristic voltage responses. However, the contribution of Cav1.2 and Cav1.3 to these voltage responses remained unknown. Hence, the relative contribution of the LTCC isoforms therein was the focus of the current study on hippocampal neurons derived from genetically modified mice, which either lack a LTCC isoform (Cav1.3 knockout mice) or express a dihydropyridine-insensitive LTCC isoform (Cav1.2DHP(-)-knockin mice). We identified common and alternate ion channel couplings of Cav1.2 and Cav1.3 channels. Whereas hyperpolarizing Ca(2+)-dependent conductances were coupled to both Cav1.2 and Cav1.3 channels, an afterdepolarizing potential was only induced by the activity of Cav1.2 channels. Unexpectedly, the activity of Cav1.2 channels was found at relatively hyperpolarized membrane voltages. Our data add important information about the differences between Cav1.2 and Cav1.3 channels that furthers our understanding of the physiological and pathophysiological neuronal roles of these calcium channels. Moreover, our findings suggest that Cav1.3 knockout mice together with Cav1.2DHP(-)-knockin mice provide valuable models for future investigation of hippocampal LTCC-dependent afterdepolarizations.
在中枢神经系统中,L 型电压门控钙通道(LTCC)有两种亚型,即 Cav1.2 和 Cav1.3 通道。先前已经表明,这些通道在生物物理特性、亚细胞定位以及与基因转录机制的偶联方面存在差异。在以前对大鼠海马神经元的研究中,我们已经确定兴奋性阳离子电导和抑制性钾电导是 LTCC 偶联的重要伙伴。值得注意的是,发现 LTCC 介导的 Ca2+内流和这些 Ca2+依赖性电导的激活之间的刺激依赖性相互作用会导致特征性的电压反应。然而,Cav1.2 和 Cav1.3 对这些电压反应的贡献仍然未知。因此,当前研究的重点是源自基因修饰小鼠的海马神经元,这些神经元要么缺乏 LTCC 亚型(Cav1.3 敲除小鼠),要么表达二氢吡啶不敏感的 LTCC 亚型(Cav1.2DHP(-)-敲入小鼠)。我们确定了 Cav1.2 和 Cav1.3 通道的共同和替代离子通道偶联。虽然去极化依赖的 Ca2+电导与 Cav1.2 和 Cav1.3 通道都偶联,但仅由 Cav1.2 通道的活动引起去极化后电位。出乎意料的是,Cav1.2 通道的活动在相对超极化的膜电压下被发现。我们的数据提供了关于 Cav1.2 和 Cav1.3 通道之间差异的重要信息,这进一步加深了我们对这些钙通道在生理和病理生理神经元作用的理解。此外,我们的发现表明,Cav1.3 敲除小鼠与 Cav1.2DHP(-)-敲入小鼠一起为未来研究海马 LTCC 依赖性后去极化提供了有价值的模型。