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1 Neurobiology and Behavior, University of California, Irvine, Irvine, California, United States
2 Anatomy and Neurobiology, University of California, Irvine, Irvine, California, United States
3 Psychiatry and Human Behavior, University of California, Irvine, Irvine, California, United States
4 Cortex Pharmaceuticals, Inc., Irvine, California, United States
5 Anatomy and Neurobiology, Neurobiology and Behavior, University of California, Irvine, Irvine, California, United States
* To whom correspondence should be addressed. E-mail: jclauter{at}uci.edu.
Restoration of neuronal viability and synaptic plasticity through increased trophic support is widely regarded as a potential therapy for the cognitive declines that characterize aging. Previous studies have shown that in the hippocampal CA1 basal dendritic field deficits in the stabilization of long term potentiation (LTP) are evident by middle age. The present study tested if increasing endogenous Brain Derived Neurotrophic Factor (BDNF) could reverse this age-related change. We report here that in middle-aged (8 to 10 month old) rats, in vivo treatments with a positive AMPA-type glutamate receptor modulator both increase BDNF protein levels in the cortical telencephalon and restore stabilization of basal dendritic LTP as assessed in acute hippocampal slices 18 hrs after the last drug treatment. These effects were not due to enhanced synaptic transmission or to facilitation of burst responses used to induce LTP. Increasing extracellular levels of BDNF via exogenous application to slices of middle-aged rats was also sufficient to rescue the stabilization of basal dendritic LTP. Finally, otherwise stable LTP in ampakine-treated, middle-aged rats can be eliminated by infusion of the extracellular BDNF scavenger TrkB-Fc. Together these results indicate that increases in endogenous BDNF signaling can offset deficits in the post-induction processes that stabilize LTP.
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