Hippocampal LTD expression involves a pool of AMPARs regulated by the NSF-GluR2 interaction

被引:242
作者
Lüthi, A [1 ]
Chittajallu, R [1 ]
Duprat, F [1 ]
Palmer, MJ [1 ]
Benke, TA [1 ]
Kidd, FL [1 ]
Henley, JM [1 ]
Isaac, JTR [1 ]
Collingridge, GL [1 ]
机构
[1] Univ Bristol, MRC, Dept Anat, Ctr Synapt Plast, Bristol BS8 1TD, Avon, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
D O I
10.1016/S0896-6273(00)80852-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated whether the interaction between the N-ethyl-maleimide-sensitive fusion protein (NSF) and the AMPA receptor (AMPAR) subunit GluR2 is involved in synaptic plasticity in the CA1 region of the hippocampus. Blockade of the NSF-GluR2 interaction by a specific peptide (pep2m) introduced into neurons prevented homosynaptic, de novo long-term depression (LTD). Moreover, saturation of LTD prevented the pep2m-induced reduction in AMPAR-mediated excitatory postsynaptic currents (EPSCs). Minimal stimulation experiments indicated that both pep2m action and LTD were due to changes in quantal size and quantal content but were not associated with changes in AMPAR single-channel conductance or EPSC kinetics. These results suggest that there is a pool of AMPARs dependent on the NSF-GluR2 interaction and that LTD expression involves the removal of these receptors from synapses.
引用
收藏
页码:389 / 399
页数:11
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