Cholecystokinin release triggered by NMDA receptors produces LTP and sound–sound associative memory
Autor: | Xiaoyu Wang, Ling He, Daisy K.Y. Shum, Jufang He, Min Li, Ailian Tan, Xia Sun, Joewel Tarra Baibado, Hui Xie, Fuqiang Xu, Nan Zhang, Yiping Guo, Robert Jesky, Zhedi Wang, Xiao Li, Yujie Peng, YS Chan, Zhijian Zhang, Zheng X, Hemin Feng, Yin Ting Wong, Jingyu Feng, Qing Liu, Zicong Zhang, Xu Zhang, Wenjian Sun, Xiaobin He, Xi Chen, Kin Lam Yung, Haitao Wang, Ling Li Hu, Micky D. Tortorella, Hon-Yeung Cheung, Junfeng Su, Kelvin Wong, Peng Tang |
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Rok vydání: | 2019 |
Předmět: |
Male
0301 basic medicine N-Methylaspartate Long-Term Potentiation Neocortex Stimulation Hippocampus Receptors N-Methyl-D-Aspartate digestive system Rats Sprague-Dawley Mice 03 medical and health sciences 0302 clinical medicine Memory medicine Animals Entorhinal Cortex Cholecystokinin Auditory Cortex Mice Knockout Neurons Multidisciplinary Behavior Animal Chemistry musculoskeletal neural and ocular physiology digestive oral and skin physiology Antagonist Long-term potentiation Electric Stimulation Receptor Cholecystokinin B Associative learning Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure PNAS Plus nervous system Synapses Cholecystokinin B receptor NMDA receptor Female Neuroscience hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery |
Zdroj: | Proceedings of the National Academy of Sciences. 116:6397-6406 |
ISSN: | 1091-6490 0027-8424 |
Popis: | 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. |
Databáze: | OpenAIRE |
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