Canzoniero L M, Rossi A, Taglialatela M, Amoroso S, Annunziato L, Di Renzo G
Department of Science of Human Communication, 2nd School of Medicine, University Federico II of Naples, Italy.
Biochim Biophys Acta. 1992 Jun 11;1107(1):175-8. doi: 10.1016/0005-2736(92)90344-l.
The activity of the Na(+)-Ca2+ exchanger, which regulates the entry and the extrusion of Ca2+ ions from nerve endings was investigated in Percoll-purified cerebrocortical synaptosomes of aged rats. 45Ca2+ uptake in a Na(+)-free medium and 45Ca2+ efflux in a 145 mM Na+ medium were significantly reduced in cerebrocortical synaptosomes from aged rats (24 months) as compared to those occurring in young (4 months) and mature (14 months) rats. 45Ca2+ influx induced by 55 mM K+, a concentration of K+ ions which selectively promotes Ca2+ entry through voltage-sensitive Ca2+ channels (VSCC), was significantly reduced in mature and aged rats as compared to that occurring in young rats. The impairment of these mechanisms in aged rats is not accompanied by any variation of fura-2 monitored Ca2+ levels under resting and depolarizing conditions.
在 Percoll 纯化的老年大鼠大脑皮质突触体中,对调节 Ca2+ 离子从神经末梢内流和外流的 Na(+)-Ca2+ 交换器活性进行了研究。与年轻(4 个月)和成熟(14 个月)大鼠相比,老年大鼠(24 个月)大脑皮质突触体在无 Na(+) 培养基中的 45Ca2+ 摄取和在 145 mM Na+ 培养基中的 45Ca2+ 流出均显著减少。由 55 mM K+ 诱导的 45Ca2+ 内流(该 K+ 离子浓度选择性促进 Ca2+ 通过电压敏感性 Ca2+ 通道(VSCC)进入),与年轻大鼠相比,在成熟和老年大鼠中显著减少。老年大鼠中这些机制的损伤在静息和去极化条件下并未伴随 fura-2 监测的 Ca2+ 水平的任何变化。