MAGUKs are essential, but redundant, in long-term potentiation

被引:14
作者
Chen, Xiumin [1 ]
Fukata, Yuko [2 ,3 ]
Fukata, Masaki [2 ,3 ]
Nicoll, Roger A. [1 ,4 ]
机构
[1] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94158 USA
[2] Natl Inst Nat Sci, Natl Inst Physiol Sci, Dept Mol & Cellular Physiol, Div Membrane Physiol, Minato, Aichi, Japan
[3] Grad Univ Adv Studies, SOKENDAI, Sch Life Sci, Dept Physiol Sci, Okazaki, Aichi 4448585, Japan
[4] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94158 USA
关键词
MAGUKs  long-term potentiation  synapse  AMPA receptors  TARPs; SYNAPTIC-TRANSMISSION; GLUTAMATE RECEPTORS; NMDA RECEPTORS; AMPA RECEPTORS; PSD-95; PLASTICITY; NEUROLIGIN-1; ARCHITECTURE; TRAFFICKING; PROTEINS;
D O I
10.1073/pnas.2107585118
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
This study presents evidence that the MAGUK family of synaptic scaffolding proteins plays an essential, but redundant, role in longterm potentiation (LTP). The action of PSD-95, but not that of SAP102, requires the binding to the transsynaptic adhesion protein ADAM22, which is required for nanocolumn stabilization. Based on these and previous results, we propose a two-step process in the recruitment of AMPARs during LTP. First, AMPARs, via TARPs, bind to exposed PSD-95 in the PSD. This alone is not adequate to enhance synaptic transmission. Second, the AMPAR/ TARP/PSD-95 complex is stabilized in the nanocolumn by binding to ADAM22. A second, ADAM22-independent pathway is proposed for SAP102.
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页数:6
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