MacKenzie G M, Jenner P, Marsden C D
Neurodegenerative Diseases Research Centre, King's College London, UK.
Neuroreport. 1995 Sep 11;6(13):1789-94. doi: 10.1097/00001756-199509000-00020.
Nitric oxide (NO) is implicated as a mediator of cell death in models of neurodegenerative disease. However, the precise role of NO in neuronal degeneration remains controversial. In the present study we employed 7-nitro indazole (7-NI), reportedly a selective inhibitor of neuronal nitric oxide synthase (nNOS) in vivo, to investigate the possible involvement of NO in quinolinic acid (QA)-induced striatal toxicity in the rat. Intrastriatal injection of QA (30 nmol) caused loss of NADPH diaphorase (48%), NOS (48%) and acetylcholinesterase (AChE; 22%) positive neurones and a loss of NOS activity (78%) in striatal homogenates. 7-NI (30 mg kg-1, i.p. every 4 h for 20 h) did not affect the loss of NADPH diaphorase (52%), NOS (52%) and AChE (16%) positive neurones or the loss of NOS activity (66%) in striatal homogenates. The present study does not support a role for NO in QA-induced striatal toxicity.
在神经退行性疾病模型中,一氧化氮(NO)被认为是细胞死亡的介质。然而,NO在神经元变性中的具体作用仍存在争议。在本研究中,我们使用了7-硝基吲唑(7-NI),据报道它在体内是神经元型一氧化氮合酶(nNOS)的选择性抑制剂,以研究NO在喹啉酸(QA)诱导的大鼠纹状体毒性中可能的作用。纹状体内注射QA(30 nmol)导致NADPH黄递酶(48%)、一氧化氮合酶(48%)和乙酰胆碱酯酶(AChE;22%)阳性神经元丧失,以及纹状体匀浆中一氧化氮合酶活性丧失(78%)。7-NI(30 mg kg-1,腹腔注射,每4小时一次,共20小时)对纹状体匀浆中NADPH黄递酶(52%)、一氧化氮合酶(52%)和乙酰胆碱酯酶(16%)阳性神经元的丧失或一氧化氮合酶活性的丧失(66%)没有影响。本研究不支持NO在QA诱导的纹状体毒性中起作用。