The oxidative stress theory of aging states that damage to molecules that are important for cellular function increases with age. This increase causes a decline in normal physiological function in a number of organs including the brain. Normal aging may be accompanied by a decline in cognitive function. It is widely believed that learning and memory are mediated by dynamic changes in the brain. Long-term potentiation (LTP) is an activity-dependent form of synaptic plasticity thought to be to be the most plausible mechanism for learning and memory. LTP was first discovered in the hippocampus, a neural structure associated with learning and memory. Interestingly, aging is accompanied by impairments in both hippocampal-dependent learning and LTP. Dietary restriction (DR) is the only environmental manipulation known to extend lifespan in all mammals studied. Many studies report that DR can prevent age-related impairments in hippocampal-dependent learning tasks. Most DR studies implement a life-long DR regimen and the animals used are adults at the time of testing. Few studies investigate the effects of short-term DR in aged rats and its consequences for learning and memory. Also, the relationship between DR and LTP longevity remains largely unexplored and no current studies document the effects of short-term DR on LTP in aged rats. The long-term goal of this research is to investigate age-related increases in oxidative brain damage, age-related deficits in hippocampal-dependent learning and medial perforant path (MPP)-CA3 LTP in awake rats, as well as their prevention by short-term (3 months) DR. In Specific Aim 1, experiments will investigate whether short-term DR can improve the performance of aged rats in trace fear conditioning and the Morris Water Maze. In Specific Aim 2, experiments will investigate whether short-term DR can extend LTP longevity in aged rats. In Specific Aim 3, experiments will investigate whether short-term DR decreases levels of oxidative brain damage and increases levels of the neuroprotective brain proteins Heat Shock Protein 70 and Brain Derived Neurotrophic Factor. These studies are expected to increase our understanding of how oxidative damage impairs hippocampal-dependent learning and LTP, how such impairments can be prevented by dietary manipulations, and whether the proposed molecular mechanisms are associated with such improvements.