Spontaneous glycine-induced calcium transients in spinal cord progenitors promote neurogenesis
- Authors
- Brustein, E., Côté, S., Ghislain, J., and Drapeau, P.
- ID
- ZDB-PUB-120815-17
- Date
- 2013
- Source
- Developmental Neurobiology 73(2): 168-175 (Journal)
- Registered Authors
- Brustein, Edna, Drapeau, Pierre, Ghislain, Julien
- Keywords
- neural progenitors, calcium transients, neurogenesis, spinal cord, zebrafish embryo
- MeSH Terms
-
- 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
- PubMed
- 22888055 Full text @ Dev. Neurobiol.
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.