Forebrain NR2B overexpression enhancing fear acquisition and long-term potentiation in the lateral amygdala
Forebrain NR2B overexpression enhancing fear acquisition and long-term potentiation in the lateral amygdala
复制标题
前脑 NR2B 过度表达增强外侧杏仁核的恐惧习得和长期增强
DOI：
10.1111/ejn.13008
复制
发表时间：
2015-09-01
影响因子：
3.4
通讯作者：
Cao, Xiaohua
中科院分区：
文献类型：
--
作者：
Duan, Yanhong;Zhou, Siqi;Cao, Xiaohua
N-methyl-d-aspartic acid (NMDA) receptor-dependent long-term potentiation (LTP) at the thalamus-lateral amygdala (T-LA) synapses is the basis for acquisition of auditory fear memory. However, the role of the NMDA receptor NR2B subunit in synaptic plasticity at T-LA synapses remains speculative. In the present study, using transgenic mice with forebrain-specific overexpression of the NR2B subunit, we have observed that forebrain NR2B overexpression results in enhanced LTP but does not alter long-term depression (LTD) at the T-LA synapses in transgenic mice. To elucidate the cellular mechanisms underlying enhanced LTP at T-LA synapses in these transgenic mice, AMPA and NMDA receptor-mediated postsynaptic currents have been measured. The data show a marked increasing in the amplitude and decay time of NMDA receptor-mediated currents in these transgenic mice. Consistent with enhanced LTP at T-LA synapses, NR2B-transgenic mice exhibit better performance in the acquisition of auditory fear memory than wild-type littermates. Our results demonstrate that up-regulation of NR2B expression facilitates acquisition of auditory cued fear memory and enhances LTP at T-LA synapses.
