Caloric restriction prevents aging-associated changes in spike-mediated Ca2+ accumulation and the slow afterhyperpolarization in hippocampal CA1 pyramidal neurons.

In hippocampal pyramidal neurons from aged animals voltage-gated Ca2+ entry and the slow, post-burst afterhyperpolarization are enhanced. As a result, there is a decrease in neuronal excitability and, in turn, an alteration in synaptic plasticity. Restricting the caloric intake of a rodent is a well-known paradigm for increasing lifespan and ameliorating a number of neurodegenerative features of aging, including deficits in synaptic plasticity and cognition. Here we show in rat CA1 pyramidal neurons from aged animals (18-20 months old) that a restricted diet prevents the enhancement of dendritic spike-mediated Ca2+ accumulation. In contrast, no significant changes in the rates of Ca2+ recovery were observed suggesting that Ca2+ clearance mechanisms are not affected by aging or caloric restriction. Lastly, we found that caloric restriction also prevented the aging-associated increase in the slow, post-burst afterhyperpolarization. Our results suggest that caloric restriction-sensitive changes in Ca2+ accumulation and membrane excitability may in part account for the protective effects of dietary restriction on synaptic plasticity and learning deficits in aged animals.