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海马突触超可塑性需要包含 NR2B 的 NMDA 受体的激活。

Hippocampal synaptic metaplasticity requires the activation of NR2B-containing NMDA receptors.

机构信息

Laboratory of Synaptic Signaling and Behavioral Neurosciences, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, PR China.

出版信息

Brain Res Bull. 2011 Feb 1;84(2):137-43. doi: 10.1016/j.brainresbull.2010.12.009. Epub 2010 Dec 22.

DOI:10.1016/j.brainresbull.2010.12.009
PMID:21184813
Abstract

The potential to exhibit synaptic plasticity itself is modulated by previous synaptic activity, which has been termed as metaplasticity. In this paper, we demonstrated that the activation of N-methyl-d-aspartate (NMDA) receptor 2B (NR2B) subunit in NNDA receptors was required for hippocampal metaplasticity at Schaffer collateral-commissural fiber-CA1 synapses. Brief 5 Hz priming stimulation did not cause long-term synaptic plasticity; however, it could result in the inhibition of subsequently evoked long-term potentiation (LTP). Meanwhile, the application of selective antagonists for NR2B subunit of NMDA receptors after delivering priming stimulation could block the metaplasticity. In contrast, LTP induction was not affected by NR2B antagonists in slices without pre-treatment of priming stimulation. These results indicated that the activation of NR2B-containing NMDA receptors was required for metaplasticity.

摘要

表现突触可塑性的潜力本身受到先前突触活动的调节,这种现象被称为易化现象。在本文中,我们证明了在海马 CA1 突触的 Schaffer 侧支-联合纤维中,需要 NMDA 受体 2B(NR2B)亚基的 N-甲基-D-天冬氨酸(NMDA)受体的激活,以实现海马的易化现象。短暂的 5 Hz 引发刺激不会导致长期的突触可塑性;然而,它可能导致随后诱发的长时程增强(LTP)的抑制。同时,在进行引发刺激后应用 NMDA 受体 NR2B 亚基的选择性拮抗剂可以阻断易化现象。相比之下,在没有进行引发刺激预处理的切片中,NR2B 拮抗剂对 LTP 的诱导没有影响。这些结果表明,NR2B 包含的 NMDA 受体的激活对于易化现象是必需的。

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