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

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