Brain-derived neurotrophic factor/TrkB signaling regulates daily ă astroglial plasticity in the suprachiasmatic nucleus: ă Electron-microscopic evidence in mouse


  • Girardet Clémence
  • Lebrun Bruno
  • Cabirol-Pol Marie-Jeanne
  • ă Tardivel Catherine
  • François-Bellan Anne-Marie
  • Becquet Denis ă
  • Bosler Olivier

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Synchronization of circadian rhythms to the 24-h light/dark (L/D) cycle ă is associated with daily rearrangements of the neuronal-glial network of ă the suprachiasmatic nucleus of the hypothalamus (SCN), the central ă master clock orchestrating biological functions in mammals. These ă anatomical plastic events involve neurons synthesizing vasoactive ă intestinal peptide (VIP), known as major integrators of photic signals ă in the retinorecipient region of the SCN. Using an analog-sensitive ă kinase allele murine model (TrkBF616A), we presently show that the ă pharmacological blockade of the tropomyosin-related kinase receptor type ă B (TrkB), the high-affinity receptor of brain-derived neurotrophic ă factor (BDNF), abolished day/night changes in the dendrite enwrapping of ă VIP neurons by astrocytic processes (glial coverage), used as an index ă of SCN plasticity on electron-microscopic sections. Therefore, the ă BDNF/TrkB signaling pathway exerts a permissive role on the ă ultrastructural rearrangements that occur in SCN under L/D alternance, ă an action that could be a critical determinant of the well-established ă role played by BDNF in the photic regulation of the SCN. In contrast, ă the extent of glial coverage of non-VIP neighboring dendrites was not ă different at daytime and nighttime in TrkBF616A mice submitted to TrkB ă inactivation or not receiving any pharmacological treatment. These data ă not only show that BDNF regulates SCN structural plasticity across the ă 24-h cycle but also reinforce the view that the daily changes in SCN ă architecture subserve the light synchronization process.

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