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依赖活动的强直性钙调神经磷酸酶活性诱导介导NMDA受体电流的快速发育性下调。

Activity-dependent induction of tonic calcineurin activity mediates a rapid developmental downregulation of NMDA receptor currents.

作者信息

Shi J, Townsend M, Constantine-Paton M

机构信息

Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.

出版信息

Neuron. 2000 Oct;28(1):103-14. doi: 10.1016/s0896-6273(00)00089-1.

DOI:10.1016/s0896-6273(00)00089-1
PMID:11086987
Abstract

Whole-cell recording in the superficial layers of the developing superior colliculus (sSC) reveals a large drop in NMDA receptor (NMDAR) current decay time synchronized across all neurons and occurring consistently between P10 and P11. We show that blocking the Ca2+/calmodulin-dependent phosphatase calcineurin (CaN) in the postsynaptic neuron can abolish this drop. The regulation is induced prematurely by 1-2 hr of electrical stimulation in P10 collicular slices only if CaN and NMDAR currents can be activated in the neuron. These data suggest that a long-lasting, CaN-mediated control of NMDAR kinetics is rapidly initiated by heightened activity of the NMDAR itself and demonstrate a novel developmental and tonic function of CaN that can play an important role in modulating the plasticity of the developing CNS.

摘要

在发育中的上丘浅层(sSC)进行全细胞记录发现,NMDA受体(NMDAR)电流衰减时间大幅下降,所有神经元同步出现,且在出生后第10天(P10)和第11天(P11)之间持续发生。我们发现,阻断突触后神经元中Ca2+/钙调蛋白依赖性磷酸酶钙调神经磷酸酶(CaN)可消除这种下降。仅当神经元中CaN和NMDAR电流能够被激活时,在P10丘脑中进行1-2小时的电刺激会过早诱导这种调节。这些数据表明,NMDAR自身活性增强会迅速启动由CaN介导的对NMDAR动力学的持久控制,并证明了CaN具有一种新的发育和紧张性功能,其在调节发育中的中枢神经系统可塑性方面可能发挥重要作用。

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