Cholecystokinin release triggered by NMDA receptors produces LTP and sound–sound associative memory

Author:

Chen Xi,Li Xiao,Wong Yin Ting,Zheng Xuejiao,Wang Haitao,Peng Yujie,Feng Hemin,Feng Jingyu,Baibado Joewel T.,Jesky Robert,Wang Zhedi,Xie Hui,Sun Wenjian,Zhang ZicongORCID,Zhang Xu,He Ling,Zhang Nan,Zhang Zhijian,Tang Peng,Su Junfeng,Hu Ling-Li,Liu Qing,He Xiaobin,Tan Ailian,Sun Xia,Li Min,Wong Kelvin,Wang Xiaoyu,Cheung Hon-Yeung,Shum Daisy Kwok-Yan,Yung Ken K. L.,Chan Ying-Shing,Tortorella Micky,Guo Yiping,Xu Fuqiang,He Jufang

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.

Funder

Research Grants Council, University Grants Committee

National Natural Science Foundation of China

FHB | Health and Medical Research Fund

Innovation and Technology Commission

National Key Basic Research Program of China

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

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