CAJ | 학술논문

目的:探讨帕金森病(Parkinson's disease, PD)大鼠模型苍白球腹侧核(ventral pallidum, VP)毁损后对旋转行为变化及对纹状体区一氧化氮合酶(nitric oxide synthase, NOS)阳性神经元表达的影响.方法:采用6-羟基多巴(6-hydroxydopamine, 6-OHDA)毁损左侧黑质致密部(substantia nigra, pars compacta, SNc)和中脑腹侧被盖(ventral tegmental area, VTA)以建立PD大鼠模型,采用微电极毁损其VP,观察实验动物旋转行为变化,并用NADPH黄递酶(reduced form of nicotinamide-edenine dinucleotide phosphate diaphorase, NADPH-d)组织化学染色显示NOS阳性神经元的表达.结果:VP毁损后PD大鼠旋转行为明显改善(P<0.05),纹状体区NOS阳性神经元数量亦有增加(P<0.05).结论:VP毁损后,PD大鼠旋转行为的减少可能与VP异常放电受抑制有关,同时NO的增加又加重了对VP的毒性损伤,从而加强了对VP异常放电的抑制作用.
목적:탐토파금삼병(Parkinson's disease, PD)대서모형창백구복측핵(ventral pallidum, VP)훼손후대선전행위변화급대문상체구일양화담합매(nitric oxide synthase, NOS)양성신경원표체적영향.방법:채용6-간기다파(6-hydroxydopamine, 6-OHDA)훼손좌측흑질치밀부(substantia nigra, pars compacta, SNc)화중뇌복측피개(ventral tegmental area, VTA)이건립PD대서모형,채용미전겁훼손기VP,관찰실험동물선전행위변화,병용NADPH황체매(reduced form of nicotinamide-edenine dinucleotide phosphate diaphorase, NADPH-d)조직화학염색현시NOS양성신경원적표체.결과:VP훼손후PD대서선전행위명현개선(P<0.05),문상체구NOS양성신경원수량역유증가(P<0.05).결론:VP훼손후,PD대서선전행위적감소가능여VP이상방전수억제유관,동시NO적증가우가중료대VP적독성손상,종이가강료대VP이상방전적억제작용.