Open AccessOpposite monosynaptic scaling of BLP–vCA1 inputs governs hopefulness- and helplessness-modulated spatial learning and memory
Author(s) -
Ying Yang,
Zhi-Hao Wang,
Sen Jin,
Di Gao,
Nan Liu,
Shan-Ping Chen,
Sinan Zhang,
Qing Liu,
Enjie Liu,
Xin Wang,
Xiao Liang,
Pengfei Wei,
Xiaoguang Li,
Lei Yin,
Chenyu Yue,
Honglian Li,
Yali Wang,
Qun Wang,
Dan Ke,
Qingguo Xie,
Fuqiang Xu,
Liping Wang,
JianZhi Wang
Publication year - 2016
Publication title -
nature communications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.559
H-Index - 365
ISSN - 2041-1723
DOI - 10.1038/ncomms11935
Subject(s) - neuroscience , optogenetics , long term potentiation , metaplasticity , excitatory postsynaptic potential , synaptic plasticity , hippocampal formation , learned helplessness , psychology , biology , receptor , developmental psychology , inhibitory postsynaptic potential , biochemistry
Different emotional states lead to distinct behavioural consequences even when faced with the same challenging events. Emotions affect learning and memory capacities, but the underlying neurobiological mechanisms remain elusive. Here we establish models of learned helplessness (LHL) and learned hopefulness (LHF) by exposing animals to inescapable foot shocks or with anticipated avoidance trainings. The LHF animals show spatial memory potentiation with excitatory monosynaptic upscaling between posterior basolateral amygdale (BLP) and ventral hippocampal CA1 (vCA1), whereas the LHL show memory deficits with an attenuated BLP–vCA1 connection. Optogenetic disruption of BLP–vCA1 inputs abolishes the effects of LHF and impairs synaptic plasticity. By contrast, targeted BLP–vCA1 stimulation rescues the LHL-induced memory deficits and mimics the effects of LHF. BLP–vCA1 stimulation increases synaptic transmission and dendritic plasticity with the upregulation of CREB and intrasynaptic AMPA receptors in CA1. These findings indicate that opposite excitatory monosynaptic scaling of BLP–vCA1 controls LHF- and LHL-modulated spatial memory, revealing circuit-specific mechanisms linking emotions to memory.