Endogenous but not sensory-driven activity controls migration, morphogenesis and survival of adult-born juxtaglomerular neurons in the mouse olfactory bulb.

Autor: Li K; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany.; Department of Physiology, University of Bern, Bern, Switzerland., Figarella K; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany., Su X; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany., Kovalchuk Y; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany., Gorzolka J; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany., Neher JJ; German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.; Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany., Mojtahedi N; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany., Casadei N; Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.; NGS Competence Center Tübingen, Tübingen, Germany., Hedrich UBS; Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany., Garaschuk O; Department of Neurophysiology, Institute of Physiology, University of Tübingen, Tübingen, Germany. olga.garaschuk@uni-tuebingen.de.
Jazyk: angličtina
Zdroj: Cellular and molecular life sciences : CMLS [Cell Mol Life Sci] 2023 Mar 18; Vol. 80 (4), pp. 98. Date of Electronic Publication: 2023 Mar 18.
DOI: 10.1007/s00018-023-04753-4
Abstrakt: The development and survival of adult-born neurons are believed to be driven by sensory signaling. Here, in vivo analyses of motility, morphology and Ca 2+ signaling, as well as transcriptome analyses of adult-born juxtaglomerular cells with reduced endogenous excitability (via cell-specific overexpression of either Kv1.2 or Kir2.1 K + channels), revealed a pronounced impairment of migration, morphogenesis, survival, and functional integration of these cells into the mouse olfactory bulb, accompanied by a reduction in cytosolic Ca 2+ fluctuations, phosphorylation of CREB and pCREB-mediated gene expression. Moreover, K + channel overexpression strongly downregulated genes involved in neuronal migration, differentiation, and morphogenesis and upregulated apoptosis-related genes, thus locking adult-born cells in an immature and vulnerable state. Surprisingly, cells deprived of sensory-driven activity developed normally. Together, the data reveal signaling pathways connecting the endogenous intermittent neuronal activity/Ca 2+ fluctuations as well as enhanced Kv1.2/Kir2.1 K + channel function to migration, maturation, and survival of adult-born neurons.
(© 2023. The Author(s).)
Databáze: MEDLINE
Externí odkaz: