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...

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Bibliographic Details
Published in:Neurobiology of aging 2010-01, Vol.31 (1), p.129-142
Main Authors: Kollen, M, Stéphan, A, Faivre-Bauman, A, Loudes, C, Sinet, P.-M, Alliot, J, Billard, J.M, Epelbaum, J, Dutar, P, Jouvenceau, A
Format: Article
Language:English
Subjects:
Aging
Aging - genetics
Aging - metabolism
Animals
Biological and medical sciences
Caloric restriction
Development. Senescence. Regeneration. Transplantation
Fundamental and applied biological sciences. Psychology
Genetic Predisposition to Disease
Hippocampus
Hippocampus - metabolism
Hippocampus - physiopathology
Insulin Resistance - genetics
Internal Medicine
Life Sciences
Male
Memory
Memory Disorders - genetics
Memory Disorders - metabolism
Memory Disorders - physiopathology
Memory, Short-Term - physiology
Neurology
Neuronal Plasticity - physiology
Neurons and Cognition
NMDA receptor
Obesity - complications
Obesity - genetics
Obesity - metabolism
Organ Culture Techniques
Rats
Rats, Inbred Strains
Rats, Sprague-Dawley
Receptors, AMPA - metabolism
Receptors, N-Methyl-D-Aspartate - metabolism
Species Specificity
Synaptic plasticity
Vertebrates: nervous system and sense organs
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Summary: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 24 h 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.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2008.03.010