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Rapid up‐regulation of the neuronal serotoninergic phenotype by brain‐derived neurotrophic factor and cyclic adenosine monophosphate: Relations with raphe astrocytes
Author(s) -
Rumajogee Prakasham,
Vergé Daniel,
Darmon Michèle,
Brisorgueil MarieJeanne,
Hamon Michel,
Miquel MarieChristine
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20572
Subject(s) - serotonergic , endocrinology , astrocyte , brain derived neurotrophic factor , tropomyosin receptor kinase b , neurotrophic factors , medicine , biology , population , neurotrophin , neurite , serotonin , microbiology and biotechnology , chemistry , neuroscience , receptor , central nervous system , biochemistry , in vitro , environmental health
Abstract Up‐regulation of the neuronal serotoninergic phenotype in relation to astrocytic population was studied in primary cultures of rat embryonic rostral raphe. Short treatments (18 hr at day in vitro 4) with brain‐derived neurotrophic factor (BDNF) or dibutyryl‐cAMP (dBcAMP) increased the number of serotoninergic neurons by ∼80% and ∼40%, respectively, and markedly enhanced the branching (by 11‐fold and 5‐fold, respectively) and total length (by 4‐fold and 2.5‐fold, respectively) of their neurites. Concomitantly, under BDNF treatment, the astrocyte population was decreased by half and became mostly protoplasmic‐like. In contrast, dBcAMP treatment also reduced the astrocytic cell density (by one‐third) but induced a stellate morphology. Similar short treatment with the astrocyte‐derived S100β factor induced no modification of the serotonin (5‐HT) neuronal phenotype nor of astrocytes morphology. Both BDNF‐ and cAMP‐induced effects were abolished by simultaneous treatment with the specific tyrosine kinase inhibitor genistein, suggesting a role for the high‐affinity BDNF receptor tyrosine kinase (TrkB). These data suggest that BDNF and cAMP, but not S100β, rapidly induce both an up‐regulation of the 5‐HT neuronal phenotype and modifications of the neighboring astrocytes in a TrkB‐dependent manner. © 2005 Wiley‐Liss, Inc.