Caloric Restriction Increases Learning Consolidation and Facilitates Synaptic Plasticity through Mechanisms Dependent on NR2B Subunits of the NMDA Receptor

One of the main focal points of aging research is the search for treatments that will prevent or ameliorate the learning and memory deficiencies associated with aging. Here we have examined the effects of maintaining mature mice on a long-term intermittent fasting diet (L-IFD). We found that L-IFD e...

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Published in:The Journal of neuroscience 2007-09, Vol.27 (38), p.10185-10195
Main Authors: Fontan-Lozano, Angela, Saez-Cassanelli, Jose Luis, Inda, Mari Carmen, de los Santos-Arteaga, Mercedes, Sierra-Dominguez, Sergio Antonio, Lopez-Lluch, Guillermo, Delgado-Garcia, Jose Maria, Carrion, Angel Manuel
Format: Article
Language:English
Subjects:
Animals
Caloric Restriction - methods
Conditioning (Psychology) - physiology
Learning - physiology
Male
Mice
Neuronal Plasticity - physiology
Receptors, N-Methyl-D-Aspartate - biosynthesis
Receptors, N-Methyl-D-Aspartate - genetics
Receptors, N-Methyl-D-Aspartate - physiology
Synapses - genetics
Synapses - metabolism
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Summary:One of the main focal points of aging research is the search for treatments that will prevent or ameliorate the learning and memory deficiencies associated with aging. Here we have examined the effects of maintaining mature mice on a long-term intermittent fasting diet (L-IFD). We found that L-IFD enhances learning and consolidation processes. We also assessed the long-term changes in synaptic efficiency in these animals. L-IFD mice showed an increase in low-theta-band oscillations, paired-pulse facilitation, and facilitation of long-term synaptic plasticity in the hippocampus with respect to mice fed ad libitum. In addition, we found an increase in the expression of the NMDA receptor subunit NR2B in some brain areas of L-IFD mice. Specific antagonism of this subunit in the hippocampus reversed the beneficial effects of L-IFD. These data provide a molecular and cellular mechanism by which L-IFD may enhance cognition, ameliorating some aging-associated cognitive deficits.
ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.2757-07.2007