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梭曼诱发癫痫发作期间脑区葡萄糖利用情况。

Brain regional glucose use during Soman-induced seizures.

作者信息

McDonough J H, Hackley B E, Cross R, Samson F, Nelson S

出版信息

Neurotoxicology. 1983 Summer;4(2):203-10.

PMID:6685261
Abstract

The (14C)-2-deoxyglucose procedure was used to determine the effects of the potent acetylcholinesterase inhibitor Soman on regional metabolism in the brain. Groups of rats were given 112 micrograms/kg Soman, 84 micrograms/kg Soman, or saline i.m., and 15 min later the (14C)-2-deoxyglucose mapping procedure was initiated. All animals given 112 micrograms/kg Soman and 2 of 6 given 84 micrograms/kg Soman developed seizures that continued throughout the mapping procedure. Very high rates of glucose use occurred in most of the brain regions studied during seizures. The most striking increases occurred in substantia nigra, septum, outer layer of dentate gyrus of the hippocampus, hippocampal body, frontal cortex, caudate, ventral thalamus, parietal cortex, medial geniculate and interpeduncular nucleus. Only the inferior colliculus, superior olivary nucleus and lateral habenula were unaffected by the seizures. The mid layers of cerebral cortex rostral to superior colliculus showed marked reductions in glucose use which may represent inhibition of neuronal activity or functional failure from depleted energy reserves. The animals given 84 micrograms/kg i.m. that did not have seizures had regional glucose use patterns similar to the controls. The results indicate that the brain damage observed by others in Soman treated rats may be in part due to the excessive neuronal stimulation that occurs during the prolonged Soman-induced seizure.

摘要

采用(14C)-2-脱氧葡萄糖法来测定强效乙酰胆碱酯酶抑制剂梭曼对脑局部代谢的影响。给大鼠分组,分别肌肉注射112微克/千克梭曼、84微克/千克梭曼或生理盐水,15分钟后开始(14C)-2-脱氧葡萄糖测绘程序。所有注射112微克/千克梭曼的动物以及6只注射84微克/千克梭曼的动物中有2只出现癫痫发作,并在整个测绘过程中持续。癫痫发作期间,大多数研究的脑区葡萄糖利用率极高。最显著的增加发生在黑质、隔区、海马齿状回外层、海马体、额叶皮质、尾状核、腹侧丘脑、顶叶皮质、内侧膝状体和脚间核。只有下丘、上橄榄核和外侧缰核未受癫痫发作的影响。上丘前方的大脑皮质中层葡萄糖利用率显著降低,这可能代表神经元活动受到抑制或能量储备耗尽导致功能衰竭。肌肉注射84微克/千克且未出现癫痫发作的动物,其局部葡萄糖利用模式与对照组相似。结果表明,其他研究中观察到的梭曼处理大鼠的脑损伤可能部分归因于梭曼诱导的长时间癫痫发作期间发生的过度神经元刺激。

相似文献

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Brain regional glucose use during Soman-induced seizures.梭曼诱发癫痫发作期间脑区葡萄糖利用情况。
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2
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引用本文的文献

1
Neurology and neuropathology of Soman-induced brain injury: an overview.梭曼致脑损伤的神经学与神经病理学概述
J Exp Anal Behav. 1994 Mar;61(2):319-29. doi: 10.1901/jeab.1994.61-319.
2
Assessment of primary neuronal culture as a model for soman-induced neurotoxicity and effectiveness of memantine as a neuroprotective drug.评估原代神经元培养作为梭曼诱导神经毒性模型的作用以及美金刚作为神经保护药物的有效性。
Arch Toxicol. 1995;69(6):384-90. doi: 10.1007/s002040050188.
3
Cerebral metabolic effects of organophosphorus anticholinesterase compounds.
有机磷抗胆碱酯酶化合物对大脑的代谢作用。
Metab Brain Dis. 1986 Jun;1(2):147-56. doi: 10.1007/BF00999384.
4
The osmotic/calcium stress theory of brain damage: are free radicals involved?脑损伤的渗透/钙应激理论:自由基参与其中吗?
Neurochem Res. 1992 Jan;17(1):11-21. doi: 10.1007/BF00966860.