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Forebrain NR 2B overexpression enhancing fear acquisition and long‐term potentiation in the lateral amygdala
Author(s) -
Duan Yanhong,
Zhou Siqi,
Ma Jing,
Yin Pengcheng,
Cao Xiaohua
Publication year - 2015
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13008
Subject(s) - long term potentiation , neuroscience , nmda receptor , forebrain , synaptic plasticity , long term depression , ampa receptor , hippocampus , amygdala , biology , chemistry , psychology , receptor , central nervous system , biochemistry
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 NR 2B subunit in synaptic plasticity at T‐ LA synapses remains speculative. In the present study, using transgenic mice with forebrain‐specific overexpression of the NR 2B subunit, we have observed that forebrain NR 2B 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, NR 2B‐transgenic mice exhibit better performance in the acquisition of auditory fear memory than wild‐type littermates. Our results demonstrate that up‐regulation of NR 2B expression facilitates acquisition of auditory cued fear memory and enhances LTP at T‐ LA synapses.