Activation of NR2B-containing NMDA receptors is not required for NMDA receptor-dependent long-term depression

被引：174

作者：

Morishita, Wade

Lu, Wei

Smith, Gordon B.

Nic, Roger A.

Bear, Mark F.

Malenka, Robert C. ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Nancy Pritzker Lab, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA

[2] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA

[4] MIT, Dept Brain & Cognit Sci, Picower Ctr Learning & Memory, Howard Hughes Med Inst, Cambridge, MA 02139 USA

来源：

NEUROPHARMACOLOGY | 2007年 / 52卷 / 01期

基金：

美国国家卫生研究院;

关键词：

long-term depression; LTD; NMDA receptors; synapses; hippocampus;

D O I：

10.1016/j.neuropharm.2006.07.005

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The triggering of both NMDA receptor-dependent long-term potentiation (LTP) and long-term depression (LTD) in the CAI region of the hippocampus requires a rise in postsynaptic calcium. A prominent hypothesis has been that the detailed properties of this postsynaptic calcium signal dictate whether LTP or LTD is generated by a given pattern of synaptic activity. Recently, however, evidence has been presented that the subunit composition of the NMDA receptor (NMDAR) determines whether a synapse undergoes LTP or LTD with NR2A-containing NMDARs triggering UP and NR2B-containing NMDARs triggering LTD. In the present study, the role of NR2B-containing synaptic NMDARs in the induction of LTD in CA1 pyramidal cells has been studied using the selective NR2B antagonists, ifenprodil and Ro25-6981. While both antagonists reduced NMDAR-mediated synaptic currents, neither prevented induction of LTD. These results demonstrate that activation of NR2B-containing NMDARs is not an absolute requirement for the induction of LTD in the hippocampus. (c) 2006 Elsevier Ltd. All rights reserved.

引用

页码：71 / 76

页数：6

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