Decreased cortical glucose utilization after ibotenate lesion of the rat ventromedial globus pallidus.
Decreased cortical glucose utilization after ibotenate lesion of the rat ventromedial globus pallidus.
复制标题
大鼠腹内侧苍白球的鹅膏酯损伤后皮质葡萄糖利用率降低。
DOI：
10.1038/jcbfm.1984.56
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Coyle,JT
中科院分区：
文献类型：
--
作者：
London,ED;McKinney,M;Dam,M;Ellis,A;Coyle,JT
在大鼠腹内侧苍白球接受鹅膏蕈氨酸（12 μg）或溶剂的单侧注射，以损害皮质胆碱能神经支配的主要来源。在注射后3或28-32天，通过2-脱氧-d-[14 C]葡萄糖技术测量9个皮质区、前丘脑和背侧海马的局部脑葡萄糖代谢率（rCMRglu）。氧化震颤素（0.1mg/kg i. p.）在鹅膏蕈氨酸损伤和假处理的大鼠中评估这些区域的rCMRgluin。鹅膏蕈氨酸注射和rCMRglu半球不对称性的显著影响在所有皮质区域中观察到（p ≤ 0.05），但在前丘脑或海马中没有观察到。在鹅膏蕈氨酸注射后3天，受损半球的皮质rCMRglu通常较低，但在假治疗后并非如此。苍白球损伤后28-32天，半球不对称性不明显。氧化震颤素在额顶叶皮层和丘脑前核产生显着影响。在额顶叶皮层，与对侧半球相比，鹅膏状突起损伤半球的rCMRglu降低了32%。Oxotremorine并没有消除半球的不对称性，但增加了38%的rCMRgluin病变额顶叶皮层。结果支持这样的观点，即在阿尔茨海默氏病皮质代谢递减部分是由于皮层下胆碱能神经支配的损失，毒蕈碱激动剂可能会部分逆转这些递减。
Rats received unilateral injections of ibotenic acid (12 μg) or vehicle in the ventromedial globus pallidus to lesion the primary source of cortical cholinergic innervation. At 3 or 28–32 days postinjection, the regional cerebral metabolic rate for glucose (rCMRglu) was measured by the 2-deoxy-d-[14C]glucose technique in nine cortical areas, the anterior thalamus, and the dorsal hippocampus. Effects of oxotremorine (0.1 mg/kg i.p.) on rCMRgluin these areas were assessed in ibotenic acid–lesioned and sham-treated rats. Significant effects of ibotenic acid injections and hemispheric asymmetries in rCMRgluwere observed in all cortical areas (p ≤ 0.05), but not in the anterior thalamus or hippocampus. Cortical rCMRglugenerally was lower in the lesioned hemisphere 3 days after ibotenic acid injections, but not after sham treatments. Hemispheric asymmetries were not apparent 28–32 days after pallidal lesions. Oxotremorine produced significant effects in the frontoparietal cortex and anterior thalamic nuclei. In the frontoparietal cortex, rCMRgluwas 32% lower in the ibotenate-lesioned hemisphere as compared with the contralateral hemisphere. Oxotremorine did not eliminate hemispheric asymmetry, but increased rCMRgluin the lesioned frontoparietal cortex by 38%. Results support the views that cortical metabolic decrements in Alzheimer's disease are due in part to loss of subcortical cholinergic innervation and that muscarinic agonists may partially reverse these decrements.