Adult Camk2a gene reinstatement restores the learning and plasticity deficits of Camk2a knockout mice

Pomme M.F. Rigter, Ilse Wallaard, Mehrnoush Aghadavoud Jolfaei, Jenina Kingma, Laura Post, Minetta Elgersma, Ype Elgersma*, Geeske M. van Woerden

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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With the recent findings that mutations in the gene encoding the α-subunit of calcium/calmodulin-dependent protein kinase II (CAMK2A) causes a neurodevelopmental disorder (NDD), it is of great therapeutic relevance to know if there exists a critical developmental time window in which CAMK2A needs to be expressed for normal brain development, or whether expression of the protein at later stages is still beneficial to restore normal functioning. To answer this question, we generated an inducible Camk2a mouse model, which allows us to express CAMK2A at any desired time. Here, we show that adult expression of CAMK2A rescues the behavioral and electrophysiological phenotypes seen in the Camk2a knock-out mice, including spatial and conditional learning and synaptic plasticity. These results suggest that CAMK2A does not play a critical irreversible role in neurodevelopment, which is of importance for future therapies to treat CAMK2A-dependent disorders.

Original languageEnglish
Article number105303
Issue number11
Publication statusPublished - 18 Nov 2022

Bibliographical note

We would like to thank Maria Smit and Armando Schoonbrood for technical assistance. This research was
supported by the NWO-VIDI (016.Vidi.188.014 to GW).

Publisher Copyright: © 2022 The Author(s)


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