The viruses used in this article are in the table below

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.

Figure. 1 HFS of CCK-containing entorhino-neocortical projections enables the association between an auditory stimulus and electrical stimulation of the auditory cortex, leading to behavioral changes.

In the present study, we used optogenetic stimulation, in vivo extracellular recordings, in vitro extracellular and intracellular recording, and behavioral testing to examine: (i) the role of CCK released from the entorhinal cortex on neocortical LTP induction and cue–cue associative memory formation, and (ii)therelationship between CCK release and NMDARs.
 
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