Journal
CELL REPORTS
Volume 4, Issue 4, Pages 738-750Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2013.07.016
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Funding
- Medical Research Council [G0500833]
- F.R.S.-F.N.R.S.
- Fonds Leon Fredericq
- Fondation Medicale Reine Elisabeth
- Belgian Science Policy (IAP-VII network) [P7/20]
- Actions de Recherche Concertees [ARC11/16-01]
- Walloon Excellence in Life Sciences and Biotechnology (WELBIO)
- Medical Research Council [G0500833, MR/J004049/1] Funding Source: researchfish
- MRC [MR/J004049/1, G0500833] Funding Source: UKRI
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Glycine receptors (GlyRs) are detected in the developing CNS before synaptogenesis, but their function remains elusive. This study demonstrates that functional GlyRs are expressed by embryonic cortical interneurons in vivo. Furthermore, genetic disruption of these receptors leads to interneuron migration defects. We discovered that extrasynaptic activation of GlyRs containing the alpha 2 subunit in cortical interneurons by endogenous glycine activates voltage-gated calcium channels and promotes calcium influx, which further modulates actomyosin contractility to fine-tune nuclear translocation during migration. Taken together, our data highlight the molecular events triggered by GlyR alpha 2 activation that control cortical tangential migration during embryogenesis.
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