海马体长时程抑制（LTD）的表达涉及由N-乙基马来酰亚胺敏感因子（NSF）与谷氨酸受体2（GluR2）相互作用所调控的一组α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPARs）。
Hippocampal LTD expression involves a pool of AMPARs regulated by the NSF-GluR2 interaction.
作者信息
Lüthi A, Chittajallu R, Duprat F, Palmer M J, Benke T A, Kidd F L, Henley J M, Isaac J T, Collingridge G L
机构信息
Medical Research Council Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, United Kingdom.
出版信息
Neuron. 1999 Oct;24(2):389-99. doi: 10.1016/s0896-6273(00)80852-1.
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.
我们研究了N - 乙基 - 马来酰亚胺敏感融合蛋白（NSF）与α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPAR）亚基GluR2之间的相互作用是否参与海马体CA1区的突触可塑性。通过导入神经元的特定肽（pep2m）阻断NSF - GluR2相互作用可防止同突触、新生的长时程抑制（LTD）。此外，LTD的饱和可防止pep2m诱导的AMPAR介导的兴奋性突触后电流（EPSC）减少。最小刺激实验表明，pep2m的作用和LTD均归因于量子大小和量子含量的变化，但与AMPAR单通道电导或EPSC动力学的变化无关。这些结果表明，存在一组依赖于NSF - GluR2相互作用的AMPAR，并且LTD的表达涉及从突触中移除这些受体。
Zotero 插件