title: Preserved memory capacities in aged Lou/C/Jall rats.
abstract: Although memory impairments are a hallmark of aging, the degree of deficit varies across animal models, and is likely to reflect different states of deterioration in metabolic and endocrinological properties. This study investigated memory-related processes in young (3-4 months) and old (24 months) Sprague-Dawley rats (SD), which develop age-linked pathologies such as obesity or insulin-resistance and Lou/C/Jall rats, which do not develop such impairments. In short- and long-term memory recognition tasks, old Lou/C/Jall rats were never impaired whereas old SD rats were deficient at 1 and 24h latencies. The expression of N-methyl-d-aspartate receptors (NMDAR)-mediated synaptic plasticity in CA1 hippocampal networks shifted towards lower activity values in old Lou/C/Jall rats whereas long-term potentiation was impaired in age-matched SD rats. Age-related decrease in NR2A subunits occurred in both strains, extended to NR2B, NR1 and GluR1 subunits in older animals (28 months) but only in SD rats. Therefore, the Lou/C/Jall rats can be considered as a model of healthy aging, not only in terms of its preserved metabolism, but also in terms of cognition and synaptic plasticity.
authors.affiliation: Centre de Psychiatrie et de Neurosciences, UMR 894 Inserm, Université Paris Descartes, Faculté de Médecine, 2 ter rue d'Alésia, F-75014 Paris, France. Kollen@broca.inserm.fr
authors.forename: M
authors.initials: M
authors.lastname: Kollen
authors.forename: A
authors.initials: A
authors.lastname: Stéphan
authors.forename: A
authors.initials: A
authors.lastname: Faivre-Bauman
authors.forename: C
authors.initials: C
authors.lastname: Loudes
authors.forename: P-M
authors.initials: PM
authors.lastname: Sinet
authors.forename: J
authors.initials: J
authors.lastname: Alliot
authors.forename: J M
authors.initials: JM
authors.lastname: Billard
authors.forename: J
authors.initials: J
authors.lastname: Epelbaum
authors.forename: P
authors.initials: P
authors.lastname: Dutar
authors.forename: A
authors.initials: A
authors.lastname: Jouvenceau
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D020022:Genetic Predisposition to Disease; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D008569:Memory Disorders / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D008570:Memory, Short-Term / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism; D009924:Organ Culture Techniques; D051381:Rats; D011919:Rats, Inbred Strains; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D013045:Species Specificity
chemical_list: D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; C409466:NR1 NMDA receptor; C120997:NR2A NMDA receptor; C121001:NR2B NMDA receptor