Entorhinal Cholecystokinin Enables Theta-Burst Stimulation-Induced Hippocampal LTP and Transfer of Spatial Memory
79 Pages Posted: 10 Sep 2019 Sneak Peek Status: Under ReviewMore...
Cholecystokinin (CCK) is purported to be involved in neuroplasticity and memory encoding. Here we found that CCK from the medial entorhinal (MEC) to hippocampus projections facilitated CA3-CA1 long-term potentiation (LTP), which further enabled spatial memory transfer. CCK knockout mice lacked theta-burst stimulation-induced CA3-CA1 LTP and their spatial memory were compromised. Upon high-frequency optical activation, the MEC CCKergic terminals in the hippocampus released CCK and induced CA3-CA1 LTP, mainly through CCK A receptors. However, down-regulation of the MEC Cck expression impaired LTP. Stimulation of hippocampal CCK neurons, the Schaffer Collaterals, or the inhibitory MEC to hippocampus terminals, induced no CA3-CA1 LTP. Activation of a group of CA1 pyramidal neurons when the mouse visited a certain place of an arena, induced primed place cells (PPCs). The CCK-strengthened connectivity of two groups of PPCs enabled the transfer of fear memory from one place to another, implicating CCK’s determining role in spatial memory encoding.
Keywords: CCKAR, long-term potentiation, spatial fear memory, temporoammonic path, primed place cells
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