Collapse of signal transduction during aging and molecular pharmacological research regarding the control.

几种不同的鸟嘌呤核苷酸调节蛋白（G蛋白）已被鉴定并在脑中探索其功能（例如Gsalpha增加腺苷酸环化酶和Ca^2+通道; Gi 1 alpha减少腺苷酸环化酶; Gi 2 alpha增加磷脂酰肌醇磷脂酶C（PI-PLC）; Gi 3 alpha增加K^+通道; Goalpha减少Ca^2+通道; Gqalpha增加PI-PLC ; G β降低腺苷酸环化酶并增加PI-PLC）。通过使用寡核苷酸探针对小鼠和大鼠大脑皮质总RNA进行杂交印迹分析，确定在同一发育期内Gsalpha和β-肌动蛋白mRNA的表达。本实验选用3、12、24月龄雄性ddy小鼠和3、6、24月龄雄性Wistar大鼠。雄性ddy小鼠和雄性Wistar大鼠的平均寿命分别为23.1和23.5个月。用硫氰酸胍/苯酚/氯仿法提取大脑皮质总RNA。两只动物的总RNA产量/组织重量在3月龄至24月龄之间没有差异。在小鼠中观察到Gsalpha蛋白mRNA（1.9kb）和β-肌动蛋白mRNA（2.0kb）的水平的年龄依赖性增加。与此相反，Gsalpha mRNA和β-肌动蛋白mRNA的水平基本相同的大鼠在老化过程中。这些结果表明，Gsalpha mRNA和β-actin mRNA的个体发育在小鼠和大鼠脑老化过程中是质的不同。

Several different guanine nucleotide regulatory proteins (G proteins) have been identified and their functions explored in brain (e.g.Gsalpha increases adenylyl cyclase and Ca^<2+> channels ; Gi1alpha decreases adenylyl cyclase : Gi2alpha increases phosphatidylinositol-phospholipase C (PI-PLC) ; Gi3alpha increases K^+ channels ; Goalpha decreases Ca^<2+> channels ; Gqalpha increases PI-PLC ; Gbeta decreases adenylyl cyclase and increases PI-PLC). The expression of Gsalpha and beta-actin mRNA was determined over the same period of development by hybridization blot analysis of total mice and rat cerebral cortex RNA using oligonucleotides for probes. Three age groups (3,12 and 24 months old) of male ddy mice and three age groups (3,6 and 24 months old) od male Wistar rats were employed in this study. The mean life spans were 23.1 and 23.5 months in male ddy mice and male Wistar rats, respecively. Total RNA from cerebral cortex was isolated by the guanidinium thiocyanate/phenol/chloroform method. Yield of total RNA/tissue weight did not differ from 3 months to 24 months of age in both animals. An age-dependent increase in the levels of Gsalpha protein mRNA (1.9kb) and beta-actin mRNA (2.0kb) was observed in the mice. In contrast, the levels of Gsalpha mRNA and beta-actin mRNA were essentially identical in the rats during aging. These results indicate that the ontogeny of Gsalpha mRNA and beta-actin mRNA between mice and rats are qualitatively different during brain aging.