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Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression
Author(s) -
Kobayashi Miwako,
Kurihara Kenzo,
Matsuoka Ichiro
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)01238-5
Subject(s) - tropomyosin receptor kinase a , tropomyosin receptor kinase b , neurotrophin , trk receptor , low affinity nerve growth factor receptor , nerve growth factor , tropomyosin receptor kinase c , retinoic acid , neurotrophin 3 , neurotrophic factors , brain derived neurotrophic factor , biology , endocrinology , medicine , receptor , microbiology and biotechnology , neuroscience , chemistry , growth factor , platelet derived growth factor receptor , cell culture , genetics
The expression of high affinity neurotrophin receptors (TrkA, TrkB, and TrkC) determines the survival response of different populations of neurons to specific members of the neurotrophin family, including nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), and neurotrophin‐3 (NT‐3). However, the mechanism which controls the expression of neurotrophin receptors during neuronal development is largely unknown. Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of trk A mRNA and induced the expression of trk B mRNA. Expression of the functional TrkB receptor was confirmed by the emergence of trophic dependence of these neurons on BDNF in the absence of NGF. Differential regulation of trk mRNAs by RA provides a possible model for the establishment of neurotrophin dependence of peripheral neurons.