Autoinactivation of neuronal AMPA receptors via glutamate-regulated TARP interaction.
Autoinactivation of neuronal AMPA receptors via glutamate-regulated TARP interaction.
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DOI：
10.1016/j.neuron.2008.11.009
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发表时间：
2009-01-15
期刊：
影响因子：
16.2
通讯作者：
Tomita, Susumu
中科院分区：
文献类型：
--
作者：
Morimoto-Tomita, Megumi;Zhang, Wei;Straub, Christoph;Cho, Chang-Hoon;Kim, Kwang S.;Howe, James R.;Tomita, Susumu
Neuronal AMPA receptors auto-inactivate at high concentrations of glutamate, i.e., the current declines at glutamate concentrations above 10–100 μM. The mechanisms underlying this phenomenon are unclear. Stargazin-like TARPs are AMPA-receptor auxiliary subunits, which modulate receptor trafficking and channel properties. Here we found that neuronal AMPA receptors and recombinant AMPA receptors co-expressed with stargazin auto-inactivate at high concentrations of glutamate, whereas recombinant AMPA receptors expressed alone do not. The reduction of currents at high glutamate concentrations is not associated with a reduction of AMPA receptor number, but rather with the loss of stargazin-associated allosteric modulation of channel gating. We show that receptor desensitization promotes the dissociation of TARP-AMPA receptor complexes in a few milliseconds. This dissociation mechanism contributes to synaptic short-term modulation. The results demonstrate a novel mechanism for dynamic regulation of AMPA receptor activity to tune synaptic strength.
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