期刊
CELL REPORTS
卷 20, 期 5, 页码 1123-1135出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.07.014
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资金
- MRC [MR/J002976/1, MR/J012998/1]
- Wellcome Trust [086185/Z/08/Z]
- NIH [K99NS094761, R01 GM113212, 1R35GM122528]
- Wellcome Trust [086185/Z/08/Z] Funding Source: Wellcome Trust
- MRC [MR/J012998/1, MR/J002976/1] Funding Source: UKRI
- Medical Research Council [MR/J002976/1, MR/J012998/1] Funding Source: researchfish
Fast excitatory transmission in the CNS is mediated mainly by AMPA-type glutamate receptors (AMPARs) associated with transmembrane AMPAR regulatory proteins (TARPs). At the high glutamate concentrations typically seen during synaptic transmission, TARPs slow receptor desensitization and enhance mean channel conductance. However, their influence on channels gated by low glutamate concentrations, as encountered during delayed transmitter clearance or synaptic spillover, is poorly understood. We report here that TARP gamma-2 reduces the ability of low glutamate concentrations to cause AMPAR desensitization and enhances channel gating at low glutamate occupancy. Simulations show that, by shifting the balance between AMPAR activation and desensitization, TARPs can markedly facilitate the transduction of spillover-mediated synaptic signaling. Furthermore, the dual effects of TARPs can account for biphasic steady-state glutamate concentration-response curves-a phenomenon termed autoinactivation,'' previously thought to reflect desensitization-mediated AMPAR/TARP dissociation.
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