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通过含GluR-B(长型)的AMPA受体的突触传递实现的谷氨酸能可塑性。

Glutamatergic plasticity by synaptic delivery of GluR-B(long)-containing AMPA receptors.

作者信息

Kolleker Alexander, Zhu J Julius, Schupp Bettina J, Qin Yi, Mack Volker, Borchardt Thilo, Köhr Georg, Malinow Roberto, Seeburg Peter H, Osten Pavel

机构信息

Max Planck Institute for Medical Research, Department of Molecular Neurobiology, Jahnstrasse 29, 69120, Heidelberg, Germany.

出版信息

Neuron. 2003 Dec 18;40(6):1199-212. doi: 10.1016/s0896-6273(03)00722-0.

DOI:10.1016/s0896-6273(03)00722-0
PMID:14687553
Abstract

Activity-driven delivery of AMPA receptors is proposed to mediate glutamatergic synaptic plasticity, both during development and learning. In hippocampal CA1 principal neurons, such trafficking is primarily mediated by the abundant GluR-A subunit. We now report a study of GluR-B(long), a C-terminal splice variant of the GluR-B subunit. GluR-B(long) synaptic delivery is regulated by two forms of activity. Spontaneous synaptic activity-driven GluR-B(long) transport maintains one-third of the steady-state AMPA receptor-mediated responses, while GluR-B(long) delivery following the induction of LTP is responsible for approximately 50% of the resulting potentiation at the hippocampal CA3 to CA1 synapses at the time of GluR-B(long) peak expression-the second postnatal week. Trafficking of GluR-B(long)-containing receptors thus mediates a GluR-A-independent form of glutamatergic synaptic plasticity in the juvenile hippocampus.

摘要

在发育和学习过程中,AMPA受体的活性驱动转运被认为可介导谷氨酸能突触可塑性。在海马CA1主神经元中,这种转运主要由丰富的GluR-A亚基介导。我们现在报告一项关于GluR-B(长型)的研究,它是GluR-B亚基的一种C末端剪接变体。GluR-B(长型)的突触转运受两种形式的活性调节。自发突触活性驱动的GluR-B(长型)转运维持了稳态AMPA受体介导反应的三分之一,而在长时程增强(LTP)诱导后GluR-B(长型)的转运在GluR-B(长型)表达峰值(出生后第二周)时,对海马CA3到CA1突触产生的约50%的增强负责。因此,含GluR-B(长型)受体的转运介导了幼年海马中一种不依赖GluR-A的谷氨酸能突触可塑性形式。

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