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Brain‐derived neurotrophic factor/TrkB signaling regulates daily astroglial plasticity in the suprachiasmatic nucleus: Electron‐microscopic evidence in mouse
Author(s) -
Girardet Clémence,
Lebrun Bruno,
CabirolPol MarieJeanne,
Tardivel Catherine,
FrançoisBellan AnneMarie,
Becquet Denis,
Bosler Olivier
Publication year - 2013
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22509
Subject(s) - tropomyosin receptor kinase b , suprachiasmatic nucleus , biology , neuroscience , brain derived neurotrophic factor , neurotrophin , neurotrophic factors , microbiology and biotechnology , medicine , endocrinology , receptor , hypothalamus , genetics
Synchronization of circadian rhythms to the 24‐h light/dark (L/D) cycle is associated with daily rearrangements of the neuronal‐glial network of the suprachiasmatic nucleus of the hypothalamus (SCN), the central master clock orchestrating biological functions in mammals. These anatomical plastic events involve neurons synthesizing vasoactive intestinal peptide (VIP), known as major integrators of photic signals in the retinorecipient region of the SCN. Using an analog‐sensitive kinase allele murine model (TrkB F616A ), we presently show that the pharmacological blockade of the tropomyosin‐related kinase receptor type B (TrkB), the high‐affinity receptor of brain‐derived neurotrophic factor (BDNF), abolished day/night changes in the dendrite enwrapping of VIP neurons by astrocytic processes (glial coverage), used as an index of SCN plasticity on electron‐microscopic sections. Therefore, the BDNF/TrkB signaling pathway exerts a permissive role on the ultrastructural rearrangements that occur in SCN under L/D alternance, an action that could be a critical determinant of the well‐established role played by BDNF in the photic regulation of the SCN. In contrast, the extent of glial coverage of non‐VIP neighboring dendrites was not different at daytime and nighttime in TrkB F616A mice submitted to TrkB inactivation or not receiving any pharmacological treatment. These data not only show that BDNF regulates SCN structural plasticity across the 24‐h cycle but also reinforce the view that the daily changes in SCN architecture subserve the light synchronization process.