This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The objective of this research program is to understand the basis of memory impairments that result from normal aging. Over the past 19 years we have discovered links between spatial memory deficits and age-related changes in hippocampal connectivity and plasticity at the cellular and network levels. While empirical focus on the hippocampus is justified because of this structures critical role in memory, the extent to which changes in upstream cortico-hippocampal inputs contribute to these age-related behavioral deficits is unknown. The perirhinal cortex is at the highest level of the ventral visual processing stream. It carries polymodal sensory information to the hippocampus, is extensively reciprocally connected with it, and is critical for memory in its own right. Whether it transmits degraded information to the aged hippocampus, resulting in deficits in visual perception or stimulus associations is thus a major question addressed in the present grant. A complementary question is whether the breakdown during aging in the connectivity and plasticity mechanisms of hippocampal circuits leads to defective associative binding among neocortical areas, and hence less robust stabilization of episodic memories. Understanding how the bidirectional interactions between these structures are altered by the aging process, and how such failures in network communication may contribute to behavioral deficits, could provide insights into the neural mechanisms of memory at all ages.
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