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Papers In Press, published online ahead of print August 4, 2003
J. Biol. Chem, 10.1074/jbc.M303082200
Submitted on March 25, 2003
Revised on July 31, 2003
Accepted on August 4, 2003

Ca2+-dependent regulation of TrkB expression in neurons

Tami J. Kingsbury, Peter D. Murray, Linda L. Bambrick, and Bruce K. Krueger

Physiology Dept., University of Maryland Medical School, Baltimore, MD 21201

Corresponding Author: tking001{at}umaryland.edu

The neurotrophin, BDNF, via activation of its receptor, trkB, regulates a wide variety of cellular processes in the nervous system including neuron survival and synaptic plasticity. Although the expression of BDNF is known to be Ca2+ dependent, the regulation of trkB expression has not been extensively studied. Here we report that depolarization of cultured mouse cortical neurons increased the expression of the full-length, catalytically active isoform of trkB without affecting expression of the truncated isoform. This increase in protein expression was accompanied by increased levels of transcripts encoding full-length, but not truncated, trkB. Depolarization also regulated transcription of the gene, TRKB, via entry of Ca2+ through voltage-gated Ca2+ channels and subsequent activation of Ca2+-responsive elements in the two TRKB promoters. Using transient transfection of neurons with TRKB promoter-luciferase constructs, we found that Ca2+ inhibited the upstream promoter P1, but activated the downstream promoter P2. Ca2+-dependent stimulation of TRKB expression requires two adjacent, non-identical CRE sites located within P2. The coordinated regulation of BDNF and trkB by Ca2+ may play a role in activity-dependent survival and synaptic plasticity by enhancing BDNF signaling in electrically active neurons.


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