Harik S I, LaManna J C, Snyder S, Wetherbee J R, Rosenthal M
Neurology. 1982 Apr;32(4):382-9. doi: 10.1212/wnl.32.4.382.
Abnormalities of cerebral oxidative metabolism were investigated in "animal models" of Parkinson disease by in situ optical measurements of local cerebral blood volume and cytochrome oxidase redox shifts in rats two weeks after unilateral 6-hydroxydopamine lesions of the substantia nigra with or without interruption of ascending noradrenergic pathways. The data demonstrate oxidative metabolic dysfunction of ipsilateral cerebral hemispheres caused by lesions that involve both dopaminergic and noradrenergic systems but not when dopaminergic neurons only are affected. We speculate that the dementia of Parkinson disease may be more prevalent when degeneration of catecholaminergic systems is widespread and not restricted to the dopaminergic system.
通过在大鼠单侧黑质6-羟基多巴胺损伤两周后，对局部脑血容量和细胞色素氧化酶氧化还原变化进行原位光学测量，在帕金森病“动物模型”中研究脑氧化代谢异常。该损伤伴有或不伴有去甲肾上腺素能上行通路的中断。数据表明，由涉及多巴胺能和去甲肾上腺素能系统的损伤引起同侧脑半球的氧化代谢功能障碍，但仅多巴胺能神经元受影响时则不会出现。我们推测，当儿茶酚胺能系统广泛退化而非仅限于多巴胺能系统时，帕金森病的痴呆可能更为普遍。
