Nishino H, Shimano Y, Kumazaki M, Sakurai T, Hida H, Fujimoto I, Fukuda A
Department of Physiology, Nagoya City University Medical School, Japan.
Neurobiology (Bp). 1995;3(3-4):257-67.
Modulation of the function of the blood-brain barrier (BBB) in the hypothalamus was investigated after the intoxication with 3-nitropropionic acid (3-NPA) that inhibits the succinate dehydrogenase. 3-NPA was administered to rats for three days. Following transcardial perfusion, brain sections were studied by immunohistochemistry. On the 2nd or 3rd day after 3-NPA, strong immunoreactions for blood-borne macromolecules, IgG, appeared in the striatum and hippocampus. Glial fibrillary acidic protein (GFAP) positive astroglias distributed heterogeneously, and induced nitric oxide synthase (iNOS) positive cells appeared around the vessels. A week later, bilateral lesions were detected in these areas. In the hypothalamus, there appeared a moderate immunoreaction for IgG, but no expression of iNOS. GFAP positive astroglias were rich especially around the vessels, and no loss in microtubule-associated protein 2 (MAP2) immunoreaction was detected, suggesting an intact BBB structure and no neuronal loss following 3-NPA intoxication. Data indicate that hypothalamic neurons are resistant to 3-NPA that induces specific lesions in the striatum and hippocampus via the damage in the BBB.
在用抑制琥珀酸脱氢酶的3-硝基丙酸（3-NPA）中毒后，研究了下丘脑血脑屏障（BBB）功能的调节。给大鼠连续三天注射3-NPA。经心脏灌注后，通过免疫组织化学研究脑切片。在3-NPA注射后的第2天或第3天，纹状体和海马中出现了对血源大分子IgG的强免疫反应。胶质纤维酸性蛋白（GFAP）阳性星形胶质细胞分布不均，血管周围出现诱导型一氧化氮合酶（iNOS）阳性细胞。一周后，在这些区域检测到双侧病变。在下丘脑中，出现了对IgG的中度免疫反应，但未检测到iNOS的表达。GFAP阳性星形胶质细胞尤其在血管周围丰富，未检测到微管相关蛋白2（MAP2）免疫反应的丧失，这表明3-NPA中毒后血脑屏障结构完整且无神经元丢失。数据表明，下丘脑神经元对3-NPA具有抗性，3-NPA通过血脑屏障损伤在纹状体和海马中诱导特定病变。
