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Loss of CaV1.3 RNA editing enhances mouse hippocampal plasticity, learning, and memory.


ABSTRACT: 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 chann

SUBMITTER: Zhai J 

PROVIDER: S-EPMC9371748 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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