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Title: Loss of CaV1.3 RNA editing enhances mouse hippocampal plasticity, learning, and memory
Creators: ZHAI JING 
NUS Contact: Jing Zhai
Subject: Neurosciences
DOI: doi:10.1073/pnas.2203883119

L-type CaV1.3 calcium channels are expressed on the dendrites and soma of neurons, and there is a paucity of information about its role in hippocampal plasticity. Here, by genetic targeting to ablate CaV1.3 RNA editing, we demonstrate that unedited CaV1.3ΔECS mice exhibited improved learning and enhanced long-term memory, supporting a functional role of RNA editing in behavior. Significantly, the editing paradox that functional recoding of CaV1.3 RNA editing sites slows Ca2+-dependent inactivation to increase Ca2+ influx but reduces channel open probability to decrease Ca2+ influx was resolved. Mechanistically, using hippocampal slice recordings, we provide evidence that unedited CaV1.3 channels permitted larger Ca2+ influx into the hippocampal pyramidal neurons to bolster neuronal excitability, synaptic transmission, late long-term potentiation, and increased dendritic arborization. Of note, RNA editing of the CaV1.3 IQ-domain was found to be evolutionarily conserved in mammals, which lends support to the importance of the functional recoding of the CaV1.3 channel in brain function.

Citation: ZHAI JING (2022-07-22). Loss of CaV1.3 RNA editing enhances mouse hippocampal plasticity, learning, and memory. ScholarBank@NUS Repository. [Dataset].
License: Attribution-NonCommercial 4.0 International
Appears in Collections:Staff Dataset

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