Ca(2+) signaling evoked by activation of Na(+) channels and Na(+)/Ca(2+) exchangers is required for GABA-induced NG2 cell migration. Tong, X., Li, X., Zhou, B., Shen, W., Zhang, Z., Xu, T., & Duan, S. The Journal of cell biology, 186(1):113–28, July, 2009. ![Ca(2+) signaling evoked by activation of Na(+) channels and Na(+)/Ca(2+) exchangers is required for GABA-induced NG2 cell migration. [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex NG2 cells originate from various brain regions and migrate to their destinations during early development. These cells express voltage-gated Na(+) channels but fail to produce typical action potentials. The physiological role of Na(+) channels in these cells is unclear. We found that GABA induces membrane depolarization and Ca(2+) elevation in NG2 cells, a process requiring activation of GABA(A) receptors, Na(+) channels, and Na(+)/Ca(2+) exchangers (NCXs), but not Ca(2+) channels. We have identified a persistent Na(+) current in these cells that may underlie the GABA-induced pathway of prolonged Na(+) elevation, which in turn triggers Ca(2+) influx via NCXs. This unique Ca(2+) signaling pathway is further shown to be involved in the migration of NG2 cells. Thus, GABAergic signaling mediated by sequential activation of GABA(A) receptors, noninactivating Na(+) channels, and NCXs may play an important role in the development and function of NG2 glial cells in the brain.
@article{Tong2009,
title = {Ca(2+) signaling evoked by activation of {Na}(+) channels and {Na}(+)/{Ca}(2+) exchangers is required for {GABA}-induced {NG2} cell migration.},
volume = {186},
issn = {1540-8140},
url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2712990&tool=pmcentrez&rendertype=abstract},
doi = {10.1083/jcb.200811071},
abstract = {NG2 cells originate from various brain regions and migrate to their destinations during early development. These cells express voltage-gated Na(+) channels but fail to produce typical action potentials. The physiological role of Na(+) channels in these cells is unclear. We found that GABA induces membrane depolarization and Ca(2+) elevation in NG2 cells, a process requiring activation of GABA(A) receptors, Na(+) channels, and Na(+)/Ca(2+) exchangers (NCXs), but not Ca(2+) channels. We have identified a persistent Na(+) current in these cells that may underlie the GABA-induced pathway of prolonged Na(+) elevation, which in turn triggers Ca(2+) influx via NCXs. This unique Ca(2+) signaling pathway is further shown to be involved in the migration of NG2 cells. Thus, GABAergic signaling mediated by sequential activation of GABA(A) receptors, noninactivating Na(+) channels, and NCXs may play an important role in the development and function of NG2 glial cells in the brain.},
number = {1},
urldate = {2013-08-10},
journal = {The Journal of cell biology},
author = {Tong, Xiao-ping and Li, Xiang-yao and Zhou, Bing and Shen, Wanhua and Zhang, Zhi-jun and Xu, Tian-le and Duan, Shumin},
month = jul,
year = {2009},
pmid = {19596850},
keywords = {\#nosource, Animals, Calcium Signaling, Calcium Signaling: drug effects, Cell Movement, Cell Movement: drug effects, Cells, Cultured, Down-Regulation, Down-Regulation: drug effects, Gramicidin, Gramicidin: pharmacology, Hippocampus, Hippocampus: cytology, Ion Channel Gating, Ion Channel Gating: drug effects, Membrane Potentials, Membrane Potentials: drug effects, RNA, Small Interfering, RNA, Small Interfering: metabolism, Rats, Rats, Sprague-Dawley, Receptors, GABA-A, Receptors, GABA-A: metabolism, Sodium, Sodium Channels, Sodium Channels: metabolism, Sodium-Calcium Exchanger, Sodium-Calcium Exchanger: metabolism, Sodium: metabolism, gamma-Aminobutyric Acid, gamma-Aminobutyric Acid: pharmacology},
pages = {113--28},
}
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