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
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