2026-04-13T03:59:02Zhttps://recercat.cat/oai/request

oai:recercat.cat:2072/4636692025-10-28T09:51:11Zcom_2072_98col_2072_378192

00925njm 22002777a 4500 dc Alemany-González, Maria author Vilademunt, Marta author Gener, Thomas author Puig, Maria Victoria author 2022 Stimulating lifestyles have powerful effects on cognitive abilities, especially when they are experienced early in life. Cognitive therapies are widely used to improve cognitive impairment due to intellectual disability, aging, and neurodegeneration, however the underlying neural mechanisms are poorly understood. We investigated the neural correlates of memory amelioration produced by postnatal environmental enrichment (EE) in diploid mice and the Ts65Dn mouse model of Down syndrome (trisomy 21). We recorded neural activities in brain structures key for memory processing, the hippocampus and the prefrontal cortex, during rest, sleep and memory performance in mice reared in non-enriched or enriched environments. Enriched wild-type animals exhibited enhanced neural synchrony in the hippocampus across different brain states (increased gamma oscillations, theta-gamma coupling, sleep ripples). Trisomic females showed increased theta and gamma rhythms in the hippocampus and prefrontal cortex across different brain states along with enlarged ripples and disrupted circuit gamma signals that were associated with memory deficits. These pathological activities were attenuated in their trisomic EE-reared peers. Our results suggest distinct neural mechanisms for the generation and rescue of healthy and pathological brain synchrony, respectively, by EE and put forward hippocampal-prefrontal hypersynchrony and miscommunication as major targets underlying the beneficial effects of EE in intellectual disability. Intellectual disability Down syndrome Prefrontal cortex Hippocampus Functional connectivity Cognitive stimulation Neural synchrony Ts65Dn Genetic mouse model Memory impairmentREM sleep Postnatal environmental enrichment enhances memory through distinct neural mechanisms in healthy and trisomic female mice