连续光照下实验性半帕金森病大鼠延髓血液循环的无能控制。

L M Shapoval, B S Kop'yak, O V Dmytrenko, V O Mayskiy, O P Mankivaska, V F Sagach
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引用次数: 0

摘要

本研究以中脑黑质多巴胺能(DA)神经元单侧损伤大鼠(实验性半帕金森病)为实验对象。多巴胺能(DA)神经元的退化伴随着对阿波啡(Apo)测试的旋转运动反应的完整神经元的过度活跃。根据旋转的次数,定义了三组动物。单侧多巴胺能(DA)神经元损伤大鼠延髓内诱导型no -合成酶(iNOS)活性显著升高,而组成型no -合成酶(cNOS)活性有降低的趋势。与对照大鼠相比,在髓核注射l -精氨酸可激活神经元no合成酶(nNOS),并伴有血流动力学效应减弱。在连续三周的光照下,动物黑质中受损的da能神经元数量增加。在此情况下,延髓中cNOS活性显著降低,导致一氧化氮(NO)的新生合成受到抑制。实验半帕金森大鼠连续光照后延髓神经元NO合成的减少也证明了这一点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
NO-ERGIC CONTROL OF BLOOD CIRCULATION IN THE MEDULLA OBLONGATA OF RATS WITH EXPERIMENTAL HEMIPARKINSONIZM UNDER EXPOSURE TO CONTINUOUS LIGHT.

The study was conducted on rats with unilateral damage to dopaminergic (DA) neurons in substantia nigra of the midbrain (experimental hemiparkinsonism). Degeneration of dopaminergic (DA) neurons was accompanied by hyperactivity of those neurons that remained intact and responded to apomorphine (Apo) test by rotational movements. Depending on the number of rotations, three groups of animals were defined. In the medulla oblongata of rats with unilateral damage to dopaminergic (DA) neurons, a significant increase in the activity of inducible NO-synthase (iNOS) was observed, while the activity of constitutive NO-synthase (cNOS) tended to decrease compared with that in control rats. An activation of neuronal NO-synthase (nNOS) in those rats by injections of L-arginine in the medullary nuclei was accompanied by weakening of the hemodynamic effects compared to those in control rats. An exposure of animals to continuous light for three weeks was accompanied by increasing the number of damaged DA-ergic neurons in substantia nigra. At that, a significant decrease in cNOS activity in the medulla oblongata was observed, leading to the inhibition of de novo synthesis of nitric oxide (NO). The reduction of NO synthesis in the medulla oblongata neurons of rats with experimental hemiparkinsonism following their exposure to continuous light was also evidenced by the reduction.

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