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首页> 外文期刊>Journal of chemical neuroanatomy >Nitric oxide synthase protein levels, not the mRNA, are downregulated in olfactory bulb interneurons of reeler mice.
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Nitric oxide synthase protein levels, not the mRNA, are downregulated in olfactory bulb interneurons of reeler mice.

机译：一氧化氮合成酶蛋白水平，而不是mRNA，在雷埃尔小鼠的嗅灯泡中间下调。

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Homozygous mutations in the Reelin gene result in severe disruption of brain development. The histogenesis of layered regions, like the neocortex, hippocampus and the cerebellum, is most notably affected in mouse reeler mutants and similar traits are also present in mice lacking molecular components of the Reelin signalling pathway. Moreover, there is evidence for an additional role of Reelin in sustaining synaptic plasticity in adult networks. Nitric oxide is an important gaseous messenger that can modulate neuronal plasticity both in developing and mature synaptic networks and has been shown to facilitate synaptic changes in the hippocampus, cerebellum and olfactory bulb. We studied the distribution and content of neuronal nitric oxide synthase in the olfactory bulbs of reeler and wildtype mice. Immunocytochemistry reveals that Reelin and neuronal nitric oxide synthase containing interneurons are two distinct, non overlapping cell populations of the olfactory bulb. We show by in situ hybridization that both nitrergic and Reelin expressing cells represent only a subset of olfactory bulb GABAergic neurons. Immunoblots show that neuronal nitric oxide synthase protein content is decreased by two thirds in reeler mice causing a detectable loss of immunolabelled cells throughout the olfactory bulb of this strain. However, neuronal nitric oxide synthase mRNA levels, essayed by quantitative real-time RT-PCR, are unaffected in the reeler olfactory bulb. Thus, disruption of the Reelin signalling pathway may modify the turnover of neuronal nitric oxide synthase in the olfactory bulb and possibly affects nitric oxide functions in reeler mice.
机译：Reelin基因中的纯合突变导致大脑发育严重破坏。层状区域的组织诱发，如Neocortex，海马和小脑，最符合在小鼠雷塞尔突变体中最符合的影响，并且在缺乏Reelin信号通路的分子组分的小鼠中也存在类似的性状。此外，有证据表明Reelin在维持成人网络中的突触可塑性方面的额外作用。一氧化氮是一种重要的气态信使，可以在开发和成熟的突触网络中调节神经元塑性，并且已被证明可以促进海马，小脑和嗅灯泡的突触变化。我们研究了雷埃尔和野生型小鼠嗅灯泡中神经元一氧化氮合酶的分布和含量。免疫细胞化学表明，含有细胞的reelin和神经元一氧化氮合酶是嗅灯泡的两个不同的非重叠细胞群。我们通过原位杂交展示，Nitreric和Reelin表达细胞只代表嗅鳞片Gabaergic神经元的子集。免疫印迹表明，雷埃尔小鼠中神经元一氧化氮合酶蛋白质含量减少了三分之二，导致在该菌株的嗅觉灯泡中可检测的免疫标签细胞的丧失。然而，通过定量实时RT-PCR的神经元一氧化氮合酶MRNA水平在re eler嗅灯泡中不受影响。因此，重组信号传导途径的破坏可以改变嗅灯泡中神经元一氧化氮合酶的转换，并且可能影响re·re erer小鼠中的一氧化氮功能。

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