Résumé
Aging is associated with alterations in different systems that govern neuronal calcium homeostasis. This study was designed to determine whether any of these alterations may contribute to the decline in spatial working memory that is observed in old rats. Several parameters [initial (5 s) and steady state (15 min)
45Ca
2+ uptake, FCCP-releaseable
45Ca
2+, [Ca
2+]
i levels, depolarization-induced phosphoprotein (P97, PP65, P42) dephosphorylation and acetylcholine levels and release) involved in calcium homeostasis/signaling were determined in whole brain synaptosomes derived from adult (9-month-old) and old (24-month-old) rats that were evaluated for spatial memory performance in the eight-arm radial maze. The neurochemical analysis indicated that both the 9- and 24-month-old rats were impaired with respect to 3-month-old animals. When learners (animals reaching criterion; RC) were compared to memory impaired rats (MI), it was found that the FCCP-releaseable
45Ca
2+ of synaptosomes, that reflects mitochondrial calcium, was lower in the MI than the RC rats was correlated with the behavioral performance of the rats in their first testing sessions. The results suggest that the loss of the calcium uptake capacity in synaptic mitochondria during aging may be associated with impaired working memory in old animals.