![]() The overexpression of RGS14414 is known to lead to increased BNDF and dendritic branching in the targeted area ( Navarro-Lobato et al., 2021 Masmudi-Martín et al., 2019) and thereby increase plasticity locally. To test if naturally restricted plasticity in the neocortex protects from memory interference, we artificially increased plasticity in the prelimbic cortex via the overexpression of an established plasticity-enhancer called regulator of G protein signaling 14 of 414 amino acids (RGS14414) ( Navarro-Lobato et al., 2021 Masmudi-Martín et al., 2019). Although these theories provide remarkable insights about learning and knowledge extraction, they remain computational models with – until now – no direct experimental support, due to the lack of a valid behavioral paradigm that enables examining structured knowledge extraction in rodents as well as interference effects. ![]() Further, the hippocampus would then still permit rapid learning of new items without disrupting this structure and therefore the dual system would protect our memories from interference when new memories would overwrite existing ones without the dual system. Computational models testing why we have a dual-learning system have proposed that the neocortex learns slowly to discover the structure in ensembles of experiences ( Marr, 1970 McClelland et al., 1995 Marr, 1971). Therefore, remote memory is based on over time accumulated neocortical changes, potentially enacted during post-training consolidation mechanisms during sleep. Neocortical synapses are less plastic and therefore are thought to change only a little on each reinstatement. Later during sleep these hippocampal representations support reactivations of recent memories in the neocortex, the ‘slow learner’ in the brain. Initially memories are stored in the hippocampus via synaptic changes in this more plastic brain area, known as the ‘fast learner’ ( Marr, 1970). ( Scoville and Milner, 1957) we know that memories are supported in the brain by a dual-learning system, but why this is the case remains unclear. Thus, we provide the first experimental evidence for the long-standing and unproven fundamental idea that high thresholds for plasticity in the cortex protect preexisting memories and modulating these thresholds affects both memory encoding and consolidation mechanisms. In contrast, hippocampal-cortical interactions in form of theta coherence during wake and REM-sleep as well as oscillatory coupling during NonREM-sleep were enhanced. Indeed, electrophysiological recordings showed that this manipulation also resulted in shorter NonREM-sleep bouts, smaller delta-waves and decreased neuronal firing rates. Here, we report that increasing plasticity via the viral-induced overexpression of RGS14414 in the prelimbic cortex leads to better one-trial memory, but that this comes at the price of increased interference in semantic-like memory. ![]() Thus, how to avoid systematic erasing of previously encoded memories? While it has been proposed that a dual-learning system with ‘slow’ learning in the cortex and ‘fast’ learning in the hippocampus could protect previous knowledge from interference, this has never been observed in the living organism. Our brain is continuously challenged by daily experiences.
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