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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Activation of constitutive nitric oxide synthase(s) and absence of inducible isoform in aged rat brain.
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Activation of constitutive nitric oxide synthase(s) and absence of inducible isoform in aged rat brain.

机译：老年大鼠脑中一氧化氮合酶的激活和诱导型亚型的缺失。

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In this study, the effect of aging on nitric oxide synthases (NOS) was investigated in homogenates and cytosolic fractions from hippocampus, brain cortex and cerebellum of adult, old adult and old Wistar rats (3-4, 14, and 24 months old, respectively). Our results indicate the enhancement of Ca(2+) and calmoduline-dependent NOS activity in all investigated aged brain parts. Significantly higher NOS activity was found in the cerebellum.In the absence of Ca(2+) or in the presence of N-nitro-L-arginine (NNLA) the activity of NOS was absent. Inhibitor of constitutive NOS isoforms which preferentially inhibits neuronal NOS (nNOS), 7-nitroindazole, decreased NOS activity by 60 and 75% in adult and aged brain, respectively. However, using RT-PCR a significantly lower amount of mRNA for nNOS was detected in hippocampus. The ratio of NOS activity to nNOS mRNA was significantly higher in hippocampus and cerebellum of aged brain. No expression of the gene for inducible NOS was observed in adult and aged brain.These results indicate that probably nNOS is responsible for higher NOS activity in aged brain. Our data suggest that alteration of nNOS phosphorylation state may be responsible for the activation of NOS in aged brain. The down-regulation of nNOS mRNA expression may be an adaptive mechanism that protects the brain against excessive NO release.
机译：在这项研究中，研究了成年，成年成年和成年Wistar大鼠（3-4、14和24个月大的大鼠）海马，大脑皮层和小脑的匀浆和胞浆中一氧化氮合酶（NOS）的衰老影响，分别）。我们的结果表明，在所有研究的老年大脑部位中，Ca（2+）和钙调素依赖性NOS活性均得到增强。在小脑中发现明显更高的NOS活性。在缺乏Ca（2+）或存在N-硝基-L-精氨酸（NNLA）的情况下，NOS的活性不存在。优先抑制神经元NOS（nNOS），7-硝基吲唑的组成型NOS同工型抑制剂在成年和老年大脑中分别降低了60％和75％的NOS活性。但是，使用RT-PCR在海马中检测到nNOS的mRNA量要低得多。在老年大脑海马和小脑中，NOS活性与nNOS mRNA的比率显着更高。在成年人和老年人的大脑中均未观察到可诱导型NOS基因的表达，这些结果表明nNOS可能是老年人脑中NOS活性较高的原因。我们的数据表明，nNOS磷酸化状态的改变可能是老年大脑中NOS活化的原因。 nNOS mRNA表达的下调可能是一种保护性机制，可保护大脑免受过量NO的释放。

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