| Literature DB >> 30850520 |
Xi Chen1,2, Xiao Li1,2, Yin Ting Wong1, Xuejiao Zheng1,2,3, Haitao Wang4, Yujie Peng1,2, Hemin Feng1, Jingyu Feng1, Joewel T Baibado1, Robert Jesky1, Zhedi Wang1,2, Hui Xie1, Wenjian Sun1, Zicong Zhang1, Xu Zhang1, Ling He1,2,5, Nan Zhang1,2, Zhijian Zhang3, Peng Tang1,2, Junfeng Su1, Ling-Li Hu4, Qing Liu3, Xiaobin He3, Ailian Tan1,2, Xia Sun6, Min Li1,2,3, Kelvin Wong1, Xiaoyu Wang1,2, Hon-Yeung Cheung1, Daisy Kwok-Yan Shum7,8, Ken K L Yung9, Ying-Shing Chan7,8, Micky Tortorella4, Yiping Guo4, Fuqiang Xu3, Jufang He10,2.
Abstract
Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK-/- mice lacked neocortical LTP and showed deficits in a cue-cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue-cue associative memory.Entities:
Keywords: NMDA receptor; cholecystokinin; entorhinal cortex; long-term potentiation; memory
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Year: 2019 PMID： 30850520 PMCID： PMC6442640 DOI： 10.1073/pnas.1816833116
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205