Abstract
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 trkA mRNA and induced the expression of trkB 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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Brain-Derived Neurotrophic Factor
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Cell Survival
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Cells, Cultured
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Nerve Growth Factors / pharmacology*
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Nerve Tissue Proteins / pharmacology*
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Neurons / drug effects*
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Neurons / metabolism
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Proto-Oncogene Proteins / biosynthesis*
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Rats
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Rats, Wistar
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Receptor Protein-Tyrosine Kinases / biosynthesis*
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Receptor, Ciliary Neurotrophic Factor
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Receptor, trkA
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Receptors, Nerve Growth Factor / biosynthesis*
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Superior Cervical Ganglion / cytology
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Superior Cervical Ganglion / drug effects
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Superior Cervical Ganglion / metabolism
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Sympathetic Nervous System / cytology
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Sympathetic Nervous System / drug effects
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Sympathetic Nervous System / metabolism
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Tretinoin / pharmacology*
Substances
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Brain-Derived Neurotrophic Factor
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Nerve Growth Factors
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Nerve Tissue Proteins
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Proto-Oncogene Proteins
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Receptor, Ciliary Neurotrophic Factor
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Receptors, Nerve Growth Factor
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Tretinoin
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Receptor Protein-Tyrosine Kinases
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Receptor, trkA