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The Journal of Neuroscience, August 6, 2008, 28(32):8034-8039; doi:10.1523/JNEUROSCI.2036-08.2008

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

Katica Boric,¹ Pablo Muñoz,¹ Michela Gallagher,² and Alfredo Kirkwood¹

¹Mind/Brain Institute and Department of Neurosciences and ²Department of Psychological and Brain Sciences, The Johns Hopkins University, Baltimore, Maryland 21218

Correspondence should be addressed to either of the following: Michela Gallagher, Department of Psychological and Brain Sciences, The Johns Hopkins University, 105 Ames Hall, 3400 North Charles Street, Baltimore, MD 21218, Email: michela{at}jhu.edu; or Alfredo Kirkwood, Mind/Brain Institute, The Johns Hopkins University, 338 Krieger Hall, 3400 North Charles Street, Baltimore, MD 21218, Email: kirkwood{at}jhu.edu

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.

Key words: learning memory; CA1; NMDA receptor; LTP; aging; senility

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Received June 25, 2008; revised June 12, 2008; accepted June 16, 2008.

Correspondence should be addressed to either of the following: Michela Gallagher, Department of Psychological and Brain Sciences, The Johns Hopkins University, 105 Ames Hall, 3400 North Charles Street, Baltimore, MD 21218, Email: michela{at}jhu.edu; or Alfredo Kirkwood, Mind/Brain Institute, The Johns Hopkins University, 338 Krieger Hall, 3400 North Charles Street, Baltimore, MD 21218, Email: kirkwood{at}jhu.edu

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