Department of Biomedical and Molecular Sciences, Graduate Program in Physiology, Centre for Neuroscience Studies, Queen's University, Kingston, Ontario K7L 3N6, Canada.
J Neurosci. 2013 Apr 10;33(15):6476-91. doi: 10.1523/JNEUROSCI.6384-11.2013.
Although the contribution of Ca(2+) buffering systems can vary between neuronal types and cellular compartments, it is unknown whether distinct Ca(2+) sources within a neuron have different buffers. As individual Ca(2+) sources can have separate functions, we propose that each is handled by unique systems. Using Aplysia californica bag cell neurons, which initiate reproduction through an afterdischarge involving multiple Ca(2+)-dependent processes, we investigated the role of endoplasmic reticulum (ER) and mitochondrial sequestration, as well as extrusion via the plasma membrane Ca(2+)-ATPase (PMCA) and Na(+)/Ca(2+) exchanger, to the clearance of voltage-gated Ca(2+) influx, Ca(2+)-induced Ca(2+)-release (CICR), and store-operated Ca(2+) influx. Cultured bag cell neurons were filled with the Ca(2+) indicator, fura-PE3, to image Ca(2+) under whole-cell voltage clamp. A 5 Hz, 1 min train of depolarizing voltage steps elicited voltage-gated Ca(2+) influx followed by EGTA-sensitive CICR from the mitochondria. A compartment model of Ca(2+) indicated the effect of EGTA on CICR was due to buffering of released mitochondrial Ca(2+) rather than uptake competition. Removal of voltage-gated Ca(2+) influx was dominated by the mitochondria and PMCA, with no contribution from the Na(+)/Ca(2+) exchanger or sarcoplasmic/endoplasmic Ca(2+)-ATPase (SERCA). In contrast, CICR recovery was slowed by eliminating the Na(+)/Ca(2+) exchanger and PMCA. Last, store-operated influx, evoked by ER depletion, was removed by the SERCA and depended on the mitochondrial membrane potential. Our results demonstrate that distinct buffering systems are dedicated to particular Ca(2+) sources. In general, this may represent a means to differentially regulate Ca(2+)-dependent processes, and for Aplysia, influence how reproductive behavior is triggered.
虽然钙缓冲系统的贡献在不同神经元类型和细胞区室之间可能有所不同,但尚不清楚神经元内的不同钙源是否具有不同的缓冲剂。由于单个钙源可以具有单独的功能,我们假设每个钙源都由独特的系统处理。使用加利福尼亚海兔袋状细胞神经元,该神经元通过涉及多个钙依赖性过程的后放电来启动繁殖,我们研究了内质网 (ER) 和线粒体隔离以及通过质膜 Ca2+-ATP 酶 (PMCA) 和 Na+/Ca2+交换体的排出对电压门控 Ca2+内流、钙诱导钙释放 (CICR) 和储存操作钙内流的清除作用。培养的袋状细胞神经元用 Ca2+指示剂 fura-PE3 填充,以在全细胞电压钳下对 Ca2+进行成像。5 Hz、1 分钟的去极化电压阶跃引发电压门控 Ca2+内流,随后线粒体产生 EGTA 敏感的 CICR。Ca2+的隔室模型表明,EGTA 对 CICR 的影响是由于缓冲释放的线粒体 Ca2+而不是摄取竞争。电压门控 Ca2+内流的消除主要由线粒体和 PMCA 控制,Na+/Ca2+交换体或肌浆/内质 Ca2+-ATP 酶 (SERCA) 没有贡献。相比之下,通过消除 Na+/Ca2+交换体和 PMCA,CICR 的恢复速度减慢。最后,通过 ER 耗竭引发的储存操作流入被 SERCA 去除,并且依赖于线粒体膜电位。我们的结果表明,不同的缓冲系统专门用于特定的钙源。一般来说,这可能代表一种差异化调节钙依赖性过程的手段,对于 Aplysia,影响生殖行为的触发方式。