Huidobro A, Blanco P, Villalba M, Gómez-Puertas P, Villa A, Pereira R, Bogónez E, Martínez-Serrano A, Aparicio J J, Satrústegui J
Department of Animal Learning Psychology, Faculty of Psychology, Complutense University of Madrid, Spain.
Neurobiol Aging. 1993 Sep-Oct;14(5):479-86. doi: 10.1016/0197-4580(93)90106-l.
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.
衰老与调控神经元钙稳态的不同系统的改变有关。本研究旨在确定这些改变是否可能导致老年大鼠空间工作记忆的下降。在来自成年（9个月大）和老年（24个月大）大鼠的全脑突触体中测定了几个参与钙稳态/信号传导的参数[初始（5秒）和稳态（15分钟）45Ca2+摄取、FCCP可释放的45Ca2+、[Ca2+]i水平、去极化诱导的磷蛋白（P97、PP65、P42）去磷酸化以及乙酰胆碱水平和释放]，这些大鼠在八臂放射状迷宫中接受了空间记忆性能评估。神经化学分析表明，9个月和24个月大的大鼠相对于3个月大的动物均存在损伤。当将学习型大鼠（达到标准的动物；RC）与记忆受损大鼠（MI）进行比较时，发现反映线粒体钙的突触体中FCCP可释放的45Ca2+在MI大鼠中低于RC大鼠，并且与大鼠在首次测试 session中的行为表现相关。结果表明，衰老过程中突触线粒体钙摄取能力的丧失可能与老年动物工作记忆受损有关。
