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Activity-dependent death of transient Cajal-Retzius neurons is required for functional cortical wiring
Journal article

Activity-dependent death of transient Cajal-Retzius neurons is required for functional cortical wiring

  • Riva, Martina Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Université de Paris, Paris, France
  • Genescu, Ioana Institut de Biologie de l’École Normale Supérieure (IBENS), Département de Biologie, École Normale Supérieure, CNRS, INSERM, Université PSL, Paris, France
  • Habermacher, Chloé INSERM U1128, Paris, France
  • Orduz, David ORCID INSERM U1128, Paris, France
  • Ledonne, Fanny Institut Jacques Monod, CNRS UMR 7592, Université de Paris, Paris, France
  • Rijli, Filippo M ORCID Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland
  • López-Bendito, Guillermina Instituto de Neurosciencias de Alicante, Universidad Miguel Hernandez, Sant Joan d’Alacant, Spain
  • Coppola, Eva Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Université de Paris, Paris, France
  • Garel, Sonia ORCID Institut de Biologie de l’École Normale Supérieure (IBENS), Département de Biologie, École Normale Supérieure, CNRS, INSERM, Université PSL, Paris, France
  • Angulo, Maria Cecilia ORCID INSERM U1128, Paris, France
  • Pierani, Alessandra ORCID Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Université de Paris, Paris, France
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  • 2019-12-31
Published in:
  • eLife. - eLife Sciences Publications, Ltd. - 2019, vol. 8
General Biochemistry, Genetics and Molecular Biology
General Immunology and Microbiology
General Neuroscience
General Medicine
English Programmed cell death and early activity contribute to the emergence of functional cortical circuits. While most neuronal populations are scaled-down by death, some subpopulations are entirely eliminated, raising the question of the importance of such demise for cortical wiring. Here, we addressed this issue by focusing on Cajal-Retzius neurons (CRs), key players in cortical development that are eliminated in postnatal mice in part via Bax-dependent apoptosis. Using Bax-conditional mutants and CR hyperpolarization, we show that the survival of electrically active subsets of CRs triggers an increase in both dendrite complexity and spine density of upper layer pyramidal neurons, leading to an excitation/inhibition imbalance. The survival of these CRs is induced by hyperpolarization, highlighting an interplay between early activity and neuronal elimination. Taken together, our study reveals a novel activity-dependent programmed cell death process required for the removal of transient immature neurons and the proper wiring of functional cortical circuits.
Language
  • English
Open access status
gold
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Persistent URL
https://sonar.ch/global/documents/11143
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