Abstract:
: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) 45Ca2+ uptake, FCCP-releaseable 45Ca2+, [Ca2+]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 45Ca2+ of synaptosomes, that reflects mitochondrial calcium, was lower in the MI than the RC rats and was correlated with the behavioral performance of the rats in their first testing sessions. The results suggest that the loss of calcium uptake capacity in synaptic mitochondria during aging may be associated with impaired working memory in old animals.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Huidobro A,Blanco P,Villalba M,Gómez-Puertas P,Villa A,Pereira R,Bogónez E,Martínez-Serrano A,Aparicio JJ,Satrústegui Jdoi
10.1016/0197-4580(93)90106-lsubject
Has Abstractpub_date
1993-09-01 00:00:00pages
479-86issue
5eissn
0197-4580issn
1558-1497pii
0197-4580(93)90106-Ljournal_volume
14pub_type
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