Potential Adaptive Function for Altered Long-Term Potentiation Mechanisms in Aging Hippocampus

Age-dependent alterations in the induction of long-term potentiation (LTP) are well documented, providing a likely neural basis for memory decline associated with aging. Studies of neural plasticity are also important to understand the neural basis of individual differences in aging, ranging from si...

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Bibliographic Details
Published in:The Journal of neuroscience 2008-08, Vol.28 (32), p.8034-8039
Main Authors: Boric, Katica, Munoz, Pablo, Gallagher, Michela, Kirkwood, Alfredo
Format: Article
Language:English
Subjects:
Adaptation, Physiological
Aging - physiology
Aging - psychology
Animals
Brief Communications
Calcium Channels, L-Type - metabolism
Cognition - physiology
Electric Stimulation
Hippocampus - physiology
In Vitro Techniques
Long-Term Potentiation - physiology
Male
Maze Learning - physiology
Memory - physiology
Neuronal Plasticity - physiology
Rats
Rats, Long-Evans
Receptors, N-Methyl-D-Aspartate - metabolism
Swimming
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Summary:Age-dependent alterations in the induction of long-term potentiation (LTP) are well documented, providing a likely neural basis for memory decline associated with aging. Studies of neural plasticity are also important to understand the neural basis of individual differences in aging, ranging from significant cognitive impairment to preservation of function on a par with younger adults. To examine the cellular mechanisms that distinguish such outcomes, we studied the induction of LTP in male outbred young and aged rats behaviorally characterized in hippocampal-dependent spatial learning. We evaluated, in vitro, the magnitude of NMDA receptor (NMDAR)-dependent and -independent forms of LTP induced in the Schaffer collateral to CA1 synapses. We found that age substantially reduces NMDAR-dependent LTP across the spectrum of cognitive outcomes, whereas increased NMDAR-independent LTP occurs distinctively in high-performing aged rats. Moreover, in young rats, behavioral performance correlates strongly with the magnitude of NMDAR-LTP, whereas NMDAR-independent LTP correlates with behavioral performance only in aged rats. Together with similar previous findings on the mechanisms for LTD in this model, these results support the notion that a shift from NMDAR-dependent to NMDAR-independent mechanisms for neural plasticity during aging is associated with better cognitive outcomes.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.2036-08.2008