ORIGINAL RESEARCH article
Front. Cell. Neurosci.
Sec. Cellular Neurophysiology
Volume 19 - 2025 | doi: 10.3389/fncel.2025.1620588
This article is part of the Research TopicMemory processing in health and disease: linking behavioral, circuits, and molecular scales.View all articles
CaMKII modulates memory destabilization by regulating the interaction of theta and gamma oscillations
Provisionally accepted
Janine Rossato
Maria Carolina Gonzalez
Johseph Souza
Andressa RadiskeGênedy ApolinárioAna Luizi Baracho
Martín Cammarota*- Brain Institute, Federal University of Rio Grande do Norte, Natal, Brazil
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Object recognition memory (ORM) allows animals to distinguish between novel and familiar items. When reactivated during recall in the presence of a novel object, a consolidated ORM can be destabilized and linked to that generated by the novel object through reconsolidation. The CA1 region of the dorsal hippocampus contributes to ORM destabilization and reconsolidation, with mechanisms involving theta/gamma crossfrequency coupling (hPAC) and synaptic plasticity modulation. Ca2+/calmodulindependent protein kinase II (CaMKII) is vital for hippocampus-dependent memory processing and has been associated with theta activity-dependent plasticity in dorsal CA1. However, the specific role of hippocampal CaMKII in the lasting storage of reactivated ORM remains unclear, and its potential impact on memory-related oscillatory activity has not been previously investigated. To explore these questions, we employed a combination of behavioral, electrophysiological, and pharmacological approaches at various stages of ORM processing, and found that CaMKII is not necessary for ORM recall or reconsolidation but does regulate novelty-induced ORM destabilization by modulating hPAC.
Keywords: Memory, reconsolidation, CaMKII, theta oscillations, gamma oscillations, Hippocampus, Memory destabilization, object recognition memory
Received: 29 Apr 2025; Accepted: 11 Aug 2025.
Copyright: © 2025 Rossato, Gonzalez, Souza, Radiske, Apolinário, Baracho and Cammarota. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Martín Cammarota, Brain Institute, Federal University of Rio Grande do Norte, Natal, RN 59056-450, Brazil
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