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在成年大鼠CA1区,长时程增强(LTP)导致N-甲基-D-天冬氨酸(NMDA)受体而非α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体的快速表面表达。

LTP leads to rapid surface expression of NMDA but not AMPA receptors in adult rat CA1.

作者信息

Grosshans D R, Clayton D A, Coultrap S J, Browning M D

机构信息

Department of Pharmacology, University of Colorado Health Science Center, 4200 E. Ninth Ave. Box C236, Denver, Colorado 80262, USA.

出版信息

Nat Neurosci. 2002 Jan;5(1):27-33. doi: 10.1038/nn779.

Abstract

In the CA1 region of the rat hippocampus, long-term potentiation (LTP) requires the activation of NMDA receptors (NMDARs) and leads to an enhancement of AMPA receptor (AMPAR) function. In neonatal hippocampus, this increase in synaptic strength seems to be mediated by delivery of AMPARs to the synapse. Here we studied changes in surface expression of native AMPA and NMDA receptors following induction of LTP in the adult rat brain. In contrast to early postnatal rats, we find that LTP in the adult rat does not alter membrane association of AMPARs. Instead, LTP leads to rapid surface expression of NMDARs in a PKC- and Src-family-dependent manner. The present study suggests a developmental shift in the LTP-dependent trafficking of AMPA receptors. Moreover, our results indicate that insertion of NMDA receptors may be a key step in regulating synaptic plasticity.

摘要

在大鼠海马体的CA1区域,长时程增强(LTP)需要NMDA受体(NMDARs)的激活,并导致AMPA受体(AMPARs)功能增强。在新生海马体中,这种突触强度的增加似乎是由AMPARs向突触的递送介导的。在此,我们研究了成年大鼠脑内诱导LTP后天然AMPA和NMDA受体表面表达的变化。与出生后早期的大鼠不同,我们发现成年大鼠的LTP不会改变AMPARs的膜结合。相反,LTP以PKC和Src家族依赖的方式导致NMDARs快速表面表达。本研究表明,AMPA受体的LTP依赖性转运存在发育转变。此外,我们的结果表明,NMDA受体的插入可能是调节突触可塑性的关键步骤。

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