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In the present work, we investigated the relationship between mitochondrial function and Ca2+ homeostasis in brain slices obtained from mice that aged normally. In acute preparations, the cerebellar neurons had similar values for intracellular free Ca2+([Ca2+]i) regardless of their age (range, 6 weeks to 24 months). However, compared with the young slices, the aged neurons (20–24 months) showed an enhanced rate of [Ca2+]i increases as a function of the time the slices were maintained in vitro. When slices were stimulated (KCl depolarization), there were significant differences in the patterns of [Ca2+]isignal displayed by the young and old cerebellar granule neurons. More importantly, the aged neurons showed a significant delay in their capacity to recover the resting [Ca2+]i. The relationship between [Ca2+]i and mitochondrial membrane potential was assessed by recording both parameters simultaneously, using fura-2 and rhodamine-123. In both young and aged neurons, the cytosolic [Ca2+]i signal was associated with a mitochondrial depolarization response. In the aged neurons, the mitochondria had a significantly longer repolarization response, and quantitative analysis showed a direct correlation between the delays in mitochondrial repolarization and [Ca2+]i recovery, indicating the causal relationship between the two parameters. Thus, the present results show that the reported changes in Ca2+homeostasis associated with aging, which manifest principally in a decreased capacity of maintaining a stable resting [Ca2+]i or recovering the resting [Ca2+]i values after stimulation, are primarily attributable to a metabolic dysfunction in which the mitochondrial impairment plays an important role.

Changes in Mitochondrial Status Associated with Altered Ca2+Homeostasis in Aged Cerebellar Granule Neurons in Brain Slices

Changes in Mitochondrial Status Associated with Altered Ca²⁺Homeostasis in Aged Cerebellar Granule Neurons in Brain Slices