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11 results on '"Delhaye, Sébastien"'

5. Defects in AMPAR trafficking and microglia activation underlie socio-cognitive deficits associated to decreased expression of phosphodiesterase 2 a

Author

Delhaye, Sébastien, primary, Jarjat, Marielle, additional, Boulksibat, Asma, additional, Sanchez, Clara, additional, Tempio, Alessandra, additional, Turtoi, Andrei, additional, Giorgi, Mauro, additional, Lacas-Gervais, Sandra, additional, Baj, Gabriele, additional, Rovere, Carole, additional, Trezza, Viviana, additional, Pellegrini, Manuela, additional, Maurin, Thomas, additional, Lalli, Enzo, additional, and Bardoni, Barbara, additional

Published
2023
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8. New Insights Into the Role of Cav2 Protein Family in Calcium Flux Deregulation in Fmr1-KO Neurons

Author

Castagnola, Sara, Delhaye, Sébastien, Folci, Alessandra, Paquet, Agnès, Brau, Frédéric, Duprat, Fabrice, Jarjat, Marielle, Grossi, Mauro, Béal, Méline, Martin, Stéphane, Mantegazza, Massimo, Bardoni, Barbara, Maurin, Thomas, Institut de pharmacologie moléculaire et cellulaire (IPMC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Laboratoire International Associé 'Neogenex' (LIA Neogenex), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-St Jude Children's Research Hospital-Hôpital Pequeño Principe, Martin, Stephane, Université Nice Sophia Antipolis (1965 - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, ratiometric calcium imaging, calcium homeostasis, [SDV]Life Sciences [q-bio], [SDV.BC]Life Sciences [q-bio]/Cellular Biology, nervous system diseases, [SDV] Life Sciences [q-bio], Cellular and Molecular Neuroscience, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, Molecular Biology, Neuroscience, Original Research, Cacna1a, Cav2.1, Fragile X syndrome
Abstract

International audience; Fragile X syndrome (FXS), the most common form of inherited intellectual disability (ID) and a leading cause of autism, results from the loss of expression of the Fmr1 gene which encodes the RNA-binding protein Fragile X Mental Retardation Protein (FMRP). Among the thousands mRNA targets of FMRP, numerous encode regulators of ion homeostasis. It has also been described that FMRP directly interacts with Ca2+ channels modulating their activity. Collectively these findings suggest that FMRP plays critical roles in Ca2+ homeostasis during nervous system development. We carried out a functional analysis of Ca2+ regulation using a calcium imaging approach in Fmr1-KO cultured neurons and we show that these cells display impaired steady state Ca2+ concentration and an altered entry of Ca2+ after KCl-triggered depolarization. Consistent with these data, we show that the protein product of the Cacna1a gene, the pore-forming subunit of the Cav2.1 channel, is less expressed at the plasma membrane of Fmr1-KO neurons compared to wild-type (WT). Thus, our findings point out the critical role that Cav2.1 plays in the altered Ca2+ flux in Fmr1-KO neurons, impacting Ca2+ homeostasis of these cells. Remarkably, we highlight a new phenotype of cultured Fmr1-KO neurons that can be considered a novel cellular biomarker and is amenable to small molecule screening and identification of new drugs to treat FXS.

Published
2018
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9. Involvement of Phosphodiesterase 2A Activity in the Pathophysiology of Fragile X Syndrome

Author

Maurin, Thomas, primary, Melancia, Francesca, additional, Jarjat, Marielle, additional, Castro, Liliana, additional, Costa, Lara, additional, Delhaye, Sébastien, additional, Khayachi, Anouar, additional, Castagnola, Sara, additional, Mota, Elia, additional, Di Giorgio, Audrey, additional, Servadio, Michela, additional, Drozd, Malgorzata, additional, Poupon, Gwénola, additional, Schiavi, Sara, additional, Sardone, Lara, additional, Azoulay, Stéphane, additional, Ciranna, Lucia, additional, Martin, Stéphane, additional, Vincent, Pierre, additional, Trezza, Viviana, additional, and Bardoni, Barbara, additional

Published
2018
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11. New Insights Into the Role of Cav2 Protein Family in Calcium Flux Deregulation in Fmr1-KO Neurons.

Author

Castagnola, Sara, Delhaye, Sébastien, Folci, Alessandra, Paquet, Agnès, Brau, Frédéric, Duprat, Fabrice, Jarjat, Marielle, Grossi, Mauro, Béal, Méline, Martin, Stéphane, Mantegazza, Massimo, Bardoni, Barbara, and Maurin, Thomas

Subjects
CALCIUM compounds, NEURON development, FRAGILE X syndrome, INTELLECTUAL disabilities, MESSENGER RNA
Abstract

Fragile X syndrome (FXS), the most common form of inherited intellectual disability (ID) and a leading cause of autism, results from the loss of expression of the Fmr1 gene which encodes the RNA-binding protein Fragile X Mental Retardation Protein (FMRP). Among the thousands mRNA targets of FMRP, numerous encode regulators of ion homeostasis. It has also been described that FMRP directly interacts with Ca2+ channels modulating their activity. Collectively these findings suggest that FMRP plays critical roles in Ca2+ homeostasis during nervous system development. We carried out a functional analysis of Ca2+ regulation using a calcium imaging approach in Fmr1-KO cultured neurons and we show that these cells display impaired steady state Ca2+ concentration and an altered entry of Ca2+ after KCl-triggered depolarization. Consistent with these data, we show that the protein product of the Cacna1a gene, the pore-forming subunit of the Cav2.1 channel, is less expressed at the plasma membrane of Fmr1-KO neurons compared to wild-type (WT). Thus, our findings point out the critical role that Cav2.1 plays in the altered Ca2+ flux in Fmr1-KO neurons, impacting Ca2+ homeostasis of these cells. Remarkably, we highlight a new phenotype of cultured Fmr1-KO neurons that can be considered a novel cellular biomarker and is amenable to small molecule screening and identification of new drugs to treat FXS. [ABSTRACT FROM AUTHOR]

Published
2018
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