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Spontaneous glycine‐induced calcium transients in spinal cord progenitors promote neurogenesis
Author(s) -
Brustein Edna,
Côté Sébastien,
Ghislain Julien,
Drapeau Pierre
Publication year - 2013
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.22050
Subject(s) - glycine receptor , strychnine , interneuron , biology , depolarization , neurogenesis , neuroscience , zebrafish , progenitor cell , population , gabaergic , spinal cord , t type calcium channel , glycine , calcium , voltage dependent calcium channel , microbiology and biotechnology , endocrinology , medicine , stem cell , biochemistry , inhibitory postsynaptic potential , environmental health , amino acid , gene
Glycine and GABA are depolarizing during early development, but the purpose of this paradoxical chloride‐mediated depolarization remains unclear, especially at early stages. It was previously reported that suppressing glycine signaling from the beginning of development in zebrafish embryos caused an abnormal maintenance of the progenitor population and a specific reduction of spinal interneurons but not of other cell populations. Here, we show that cells including progenitors in the embryonic spinal cord had occasional spontaneous, glycine‐mediated calcium transients that were blocked by the glycine antagonist strychnine and the L‐type calcium channel blocker nifedipine. As shown previously for chronic block by strychnine, block of these transients by nifedipine reduced interneuron differentiation. Our results indicate that glycinergic depolarization of neural progenitors evokes spontaneous calcium transients that may enhance the interneuron neurogenic program. © 2012 Wiley Periodicals, Inc. Develop Neurobiol, 2013