Open AccessR-Type Calcium Channels Are Crucial for Semaphorin 3A–Induced DRG Axon Growth Cone Collapse
Author(s) -
Rimantas Treinys,
Andrius Kaselis,
Emmanuel Jover,
Dominique Bagnard,
Saulius Šatkauskas
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0102357
Subject(s) - sema3a , semaphorin , growth cone , intracellular , microbiology and biotechnology , extracellular , calcium in biology , axon guidance , biology , neuroscience , calcium channel , voltage dependent calcium channel , channel blocker , calcium , t type calcium channel , axon , biophysics , chemistry , medicine , biochemistry , receptor
Semaphorin 3A (Sema3A) is a secreted protein involved in axon path-finding during nervous system development. Calcium signaling plays an important role during axonal growth in response to different guidance cues; however it remains unclear whether this is also the case for Sema3A. In this study we used intracellular calcium imaging to figure out whether Sema3A-induced growth cone collapse is a Ca 2+ dependent process. Intracellular Ca 2+ imaging results using Fura-2 AM showed Ca 2+ increase in E15 mice dorsal root ganglia neurons upon Sema3A treatment. Consequently we analyzed Sema3A effect on growth cones after blocking or modifying intracellular and extracellular Ca 2+ channels that are expressed in E15 mouse embryos. Our results demonstrate that Sema3A increased growth cone collapse rate is blocked by the non-selective R- and T- type Ca 2+ channel blocker NiCl 2 and by the selective R-type Ca 2+ channel blocker SNX482 . These Ca 2+ channel blockers consistently decreased the Sema3A-induced intracellular Ca 2+ concentration elevation. Overall, our results demonstrate that Sema3A-induced growth cone collapses are intimately related with increase in intracellular calcium concentration mediated by R-type calcium channels.