Reference - Detail
|Author||Brustein E, Côté S, Ghislain J, Drapeau P.|
|Title||Spontaneous glycine-induced calcium transients in spinal cord progenitors promote neurogenesis.|
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.
|MeSH||Animals Calcium Channel Blockers / pharmacology Calcium Signaling / drug effects* Cell Differentiation / drug effects Cell Differentiation / physiology Data Interpretation, Statistical Embryo, Nonmammalian Glycine / pharmacology* Glycine Agents / pharmacology Green Fluorescent Proteins Immunohistochemistry Interneurons / physiology Microscopy, Confocal Neural Stem Cells / drug effects* Neurogenesis / drug effects* Nifedipine / pharmacology Spinal Cord / cytology Spinal Cord / drug effects* Spinal Cord / growth & development* Strychnine / pharmacology Zebrafish|
|WOS Category||DEVELOPMENTAL BIOLOGY NEUROSCIENCES|