Rap2-JNK removes synaptic AMPA receptors during depotentiation

被引：168

作者：

Zhu, YH

Pak, D

Qin, Y

McCormack, SG

Kim, MJ

Baumgart, JP

Velamoor, V

Auberson, YR

Osten, P

van Aelst, L

Sheng, M

Zhu, JJ ^{[1
]}

机构：

[1] Univ Virginia, Sch Med, Dept Pharmacol, Charlottesville, VA 22908 USA

[2] Univ Virginia, Sch Med, Grad Program Neurosci, Charlottesville, VA 22908 USA

[3] MIT, Ctr Res Neurosci, RIKEN, Howard Hughes Med Inst,Picower Ctr Learning & Mem, Cambridge, MA 02139 USA

[4] Cold Spring Harbor Lab, Canc Res Ctr, Cold Spring Harbor, NY 11724 USA

[5] Novartis Pharma AG, Novartis Inst Biomed Res, CH-4002 Basel, Switzerland

[6] Max Planck Inst Med Res, Dept Mol Neurobiol, D-69120 Heidelberg, Germany

来源：

NEURON | 2005年 / 46卷 / 06期

关键词：

D O I：

10.1016/j.neuron.2005.04.037

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The related small GTPases Ras and Rap1 are important for signaling synaptic AMPA receptor (-R) trafficking during long-term potentiation (LTP) and longterm depression (LTD), respectively. Rap2, which shares 60% identity to Rap1, is present at excitatory synapses, but its functional role is unknown. Here, we report that Rap2 activity, stimulated by NR2A-containing NMDA-R activation, depresses AMPA-R-mediated synaptic transmission via activation of JNK rather than Erk1/2 or p38 MAPK. Moreover, Rap2 controls synaptic removal of AMPA-Rs with long cytoplasmic termini during depotentiation. Thus, Rap2-JNK pathway, which opposes the action of the NR2A-containing NMDA-R-stimulated Ras-ERK1/2 signaling and complements the NR2B-containing NMDA-R-stimulated Rapl-p38 MAPK signaling, channels

引用

页码：905 / 916

页数：12

共 50 条

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