Letter to NeuroscienceBrain-derived neurotrophic factor regulates the expression of AMPA receptor proteins in neocortical neurons
Section snippets
Discussion
In the present study, our results suggest that BDNF can increase specifically protein levels of AMPA receptors. Reversibly, expression of BDNF itself is known to be induced by activation of AMPA receptors in the brain.11, 35Therefore, these two observations indicate that BDNF and AMPA receptors mutually interact with each other to regulate positively the other expression. Their interactions might contribute to normal brain development and plasticity.23, 33
The receptor increase appeared to occur
Acknowledgements
We thank Dr P. Ernfors and Dr R. Jaenisch for providing the brain tissues from BDNF mutant mice, Miss J. H. Kogan and Mrs C. Fujikawa for technical assistance, Dr S. Heinemann for rat GluR1 cDNA, Dr K. Sakimura for mouse GluR2 cDNA and GluR2/3 antibodies, and Dr T. Yamamoto for his advice. This project was supported by the Japan Society for the Promotion of Science (RFTF-96L00203).
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2015, NeuropharmacologyCitation Excerpt :Tropomyosin receptor kinase B (TrkB), the high affinity receptor of brain-derived neurotrophic factor (BDNF) and neurotrophin-3/4 ligands, is located on axon terminals and in the post-synaptic density of glutamatergic synapses (Drake et al., 1999; Aoki et al., 2000; Pereira et al., 2006). Several studies indicated that the interaction of TrkB and BDNF up-regulates protein levels of AMPAR subunits in the neurons, and induces the delivery of AMPARs to the synapse (Nakamoto et al., 2007; Narisawa-Saito et al., 1999, 2002; Caldeira et al., 2007; Jourdi and Kabbaj, 2013). We therefore hypothesized that dysregulation of synaptic transmission and memory impairment in FXS could be improved by modulating AMPARs through acting on TrkB.