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Brain‐derived neurotrophic factor regulates AMPA receptor trafficking to post‐synaptic densities via IP3R and TRPC calcium signaling
Author(s) -
Nakata Hiroko,
Nakamura Shun
Publication year - 2007
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/j.febslet.2007.04.041
Subject(s) - trpc , ampa receptor , microbiology and biotechnology , synaptic plasticity , neurotrophic factors , chemistry , brain derived neurotrophic factor , glutamatergic , neuroscience , transient receptor potential channel , calcium signaling , biology , glutamate receptor , receptor , signal transduction , biochemistry
The change in the number of post‐synaptic α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA)‐type glutamatergic receptors (AMPARs) by neuronal activity is recognized as a molecular basis of synaptic plasticity. Here, we show that Ca 2+ transients evoked by brain‐derived neurotrophic factor (BDNF) induce translocation of a subunit of AMPAR, GluR1, but not NMDAR, to the post‐synaptic membrane in cultured cortical pyramidal neurons. Among BDNF‐induced Ca 2+ transients, that dependent on IP3R was fully required, while store‐operated calcium influx through the non‐selective cation channel TRPC (transient receptor potential canonical) was partially required for the GluR1 up‐regulation, suggesting that spatial and temporal calcium signaling regulate translocation of GluR1 to the polarized membrane domain.