کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3070727 | 1580753 | 2006 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: A genetic approach using knockout mice Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: A genetic approach using knockout mice](/preview/png/3070727.png)
The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS−/−) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, quantitative [14C]iodoantipyrine method) was measured 3–6 h after unilateral kainate (KA) injection in the dorsal hippocampus; controls received saline. In WT mice, KA seizures induced a 22 to 50% LCBF increase restricted to the ipsilateral hippocampus, while significant LCBF decreases (15–33%) were noticed in 22% of the contralateral areas, i.e., the parietal cortex, amygdala and three basal ganglia areas, compared to saline-injected WT mice. In eNOS−/− mice, no LCBF increases were recorded within the epileptic focus and generalized contralateral LCBF decreases (22–46%) were noticed in 2/3 of the brain areas, compared to saline-injected eNOS−/− mice. Thus, endothelial NO is the mediator of the cerebrovascular response within the epileptic focus and participates in the maintenance of LCBF in distant areas.
Journal: Neurobiology of Disease - Volume 23, Issue 1, July 2006, Pages 219–227