Brain-derived neurotrophic factor regulates AMPA receptor trafficking to post-synaptic densities via IP3R and TRPC calcium signaling

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• 作者：Hiroko Nakata ; Shun Nakamura
• 关键词：GluR1 ; Cortical pyramidal neuron ; PSD-95 ; PLC-γ ; Dendrite ; Spine
• 刊名：FEBS Letters
• 出版年：2007
• 期刊代码：70_00145793
• 类别：bio
• 出版时间：15 May 2007
• 卷：581
• 期：10
• 页码：2047-2054
• 文件大小：363 K

摘要

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 Ca²⁺ 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 Ca²⁺ 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.