Regulation of radial glial process growth by glutamate via mGluR5/TRPC3 and neuregulin/ErbB4.
Autor: | Louhivuori LM; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland.; Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, SE-171 77, Sweden., Turunen PM; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland., Louhivuori V; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland., Yellapragada V; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland., Nordström T; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland., Uhlén P; Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, SE-171 77, Sweden., Åkerman KE; University of Helsinki, Biomedicum, Medicum/Physiology, Helsinki, FIN-00014, Finland. |
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Jazyk: | angličtina |
Zdroj: | Glia [Glia] 2018 Jan; Vol. 66 (1), pp. 94-107. Date of Electronic Publication: 2017 Sep 09. |
DOI: | 10.1002/glia.23230 |
Abstrakt: | Radial glial cells play an essential role through their function as guides for neuronal migration during development. Disruption of metabotropic glutamate receptor 5 (mGluR5) function retards the growth of radial glial processes in vitro. Neuregulins (NRG) are activated by proteolytic cleavage and regulate (radial) glial maintenance via ErbB3/ErbB4 receptors. We show here that blocking ErbB4 disrupts radial process extension. Soluble NRG acting on ErbB4 receptors is able to promote radial process extension in particular where process elongation has been impeded by blockade of mGluR5, the nonselective cation channel canonical transient receptor potential 3 (TRPC3), or matrix metalloproteases (MMP). NRG does not restore retarded process growth caused by ErbB4 blockade. Stimulation of muscarinic receptors restores process elongation due to mGluR5 blockade but not that caused by TRPC3, MMP or ErbB4 blockade suggesting that muscarinic receptors can replace mGluR5 with respect to radial process extension. Additionally, NRG/ErbB4 causes Ca 2+ mobilization in a population of cells through cooperation with ErbB1 receptors. Our results indicate that mGluR5 promotes radial process growth via NRG activation by a mechanism involving TRPC3 channels and MMPs. Thus neurotransmitters acting on G-protein coupled receptors could play a central role in the maintenance of the radial glial scaffold through activation of NRG/ErbB4 signaling. (© 2017 Wiley Periodicals, Inc.) |
Databáze: | MEDLINE |
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