Changes of calcium homeostasis in nerve endings during aging

Calcium uptake reduction in synaptosomes observed in old rats is partly due to a decreased calcium influx through brain voltage-dependent calcium channels. This defect is not due to differences in the polarization of the plasma membrane, but rather to the influx of calcium itself, and may be accentuated at lower concentrations of calcium. We found that the cytosolic calcium concentration in 24-month-old rats is higher than in adults, both at rest and under K-depolarization, and it is suggested that these high calcium levels may partially inactivate synaptosomal calcium channels. The mitochondrial defect may be partially responsible for the increase in cytosolic calcium with age in K-depolarized synaptosomes, but other factors are probably responsible for the increase in resting (Ca2+).