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.
journal_name
Proc Natl Acad Sci U S Aauthors
Chen X,Li X,Wong YT,Zheng X,Wang H,Peng Y,Feng H,Feng J,Baibado JT,Jesky R,Wang Z,Xie H,Sun W,Zhang Z,Zhang X,He L,Zhang N,Zhang Z,Tang P,Su J,Hu LL,Liu Q,He X,Tan A,Sun X,Li M,Wong K,Wang X,Cheungdoi
10.1073/pnas.1816833116subject
Has Abstractpub_date
2019-03-26 00:00:00pages
6397-6406issue
13eissn
0027-8424issn
1091-6490pii
1816833116journal_volume
116pub_type
杂志文章abstract::The human epidermal growth factor receptor 2 (HER2) is specifically overexpressed in tumors of several cancers, including an aggressive form of breast cancer. It is therefore a target for both cancer diagnostics and therapy. The 58 amino acid residue Zher2 affibody molecule was previously engineered as a high-affinity...
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