Involvement of hippocampal synaptic plasticity in age-related memory decline.
This article examines the functional significance of Ca(2+)-dependent synaptic plasticity in relation to compromised memory function during aging. Research characterizing an age-related decline in memory for tasks that require proper hippocampal function is summarized. It is concluded that aged animals possess the mechanisms necessary for memory formation, and memory deficits, including rapid forgetting, result from more subtle changes in memory processes for memory storage or maintenance. A review of experimental studies concerning changes in hippocampal neural plasticity over the course of aging indicates that, during aging, there is a shift in mechanisms that regulate the thresholds for synaptic modification, including Ca(2+) channel function and subsequent Ca(2+)-dependent processes. The results, combined with theoretical considerations concerning synaptic modification thresholds, provide the basis for a model of age-related changes in hippocampal synaptic function. The model is employed as a foundation for interpretation of studies examining therapeutic intervention in age-related memory decline. The possible role of altered synaptic plasticity thresholds in learning and memory deficits suggests that treatments that modify synaptic plasticity may prove fruitful for the development of early therapeutic interventions in age-related neurodegenerative diseases.
Foster
T C
TC
Department of Pharmacology, College of Medicine, University of Kentucky, MS-305 UKMC, Lexington, KY, USA. tfoster@pop.uky.edu
D000375:Aging / Q000502:physiology*; D000818:Animals; D015220:Calcium Channels / Q000502:physiology; D006624:Hippocampus / Q000502:physiology*; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology; D008569:Memory Disorders / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D013569:Synapses / Q000502:physiology*
D015220:Calcium Channels