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创伤性损伤可诱导脊髓神经元中的神经元型一氧化氮合酶。

Neuronal nitric oxide synthase is induced in spinal neurons by traumatic injury.

作者信息

Wu W, Liuzzi F J, Schinco F P, Depto A S, Li Y, Mong J A, Dawson T M, Snyder S H

机构信息

Department of Neurosurgery, Eastern Virginia Medical School, Norfolk 23501.

出版信息

Neuroscience. 1994 Aug;61(4):719-26. doi: 10.1016/0306-4522(94)90394-8.

DOI:10.1016/0306-4522(94)90394-8
PMID:7530816
Abstract

Nitric oxide appears to mediate the immune functions of macrophages, the influence of endothelial cells on blood vessel relaxation, and also to serve as a neurotransmitter in the central and peripheral nervous system. Macrophage nitric oxide synthase is inducible with massive increases in new nitric oxide synthase protein synthesis following immune stimulation of macrophages. By contrast, endothelial nitric oxide synthase and neuronal nitric oxide synthase are thought to be constitutive with activation induced by calcium entry into cells in the absence of new protein synthesis. Developmental studies showing the transient expression of neuronal nitric oxide synthase in embryonic and early postnatal life in rodent spinal motoneurons and cerebral cortical plate neurons (Bredt and Snyder, unpublished observations) implies inducibility of neuronal nitric oxide synthase. Moreover, neuronal nitric oxide synthase expression is greatly enhanced in sensory ganglia following peripheral axotomy. Staining for NADPH diaphorase in spinal motoneurons is greatly increased following ventral root avulsion. In many parts of the Central Nervous System NADPH diaphorase staining reflects nitric oxide synthase. In the present study, we have combined in situ hybridization for neuronal nitric oxide synthase, immunohistochemical staining of neuronal nitric oxide synthase, and NADPH diaphorase staining to establish that neuronal nitric oxide synthase expression is markedly augmented in spinal motoneurons following avulsion. The generality of this effect is evident from augmented staining in nucleus dorsalis following spinal cord transection.

摘要

一氧化氮似乎介导巨噬细胞的免疫功能、内皮细胞对血管舒张的影响,并且还在中枢和外周神经系统中充当神经递质。巨噬细胞一氧化氮合酶是可诱导的,在巨噬细胞受到免疫刺激后,新的一氧化氮合酶蛋白合成会大量增加。相比之下,内皮型一氧化氮合酶和神经元型一氧化氮合酶被认为是组成型的,在没有新蛋白质合成的情况下,通过钙离子进入细胞诱导激活。发育研究表明,啮齿动物脊髓运动神经元和大脑皮质板神经元在胚胎期和出生后早期短暂表达神经元型一氧化氮合酶(布雷特和斯奈德,未发表的观察结果),这意味着神经元型一氧化氮合酶具有可诱导性。此外,外周轴突切断后,感觉神经节中神经元型一氧化氮合酶的表达会大大增强。腹根撕脱后,脊髓运动神经元中NADPH黄递酶的染色大大增加。在中枢神经系统的许多部位,NADPH黄递酶染色反映一氧化氮合酶。在本研究中,我们结合了神经元型一氧化氮合酶的原位杂交、神经元型一氧化氮合酶的免疫组织化学染色和NADPH黄递酶染色,以确定撕脱后脊髓运动神经元中神经元型一氧化氮合酶的表达明显增强。脊髓横断后背核染色增强,表明这种效应具有普遍性。

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Neuronal nitric oxide synthase is induced in spinal neurons by traumatic injury.创伤性损伤可诱导脊髓神经元中的神经元型一氧化氮合酶。
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