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在小鼠大脑中动脉闭塞后核心区和半影区的代谢和递质变化。

Metabolic and transmitter changes in core and penumbra after middle cerebral artery occlusion in mice.

机构信息

Department of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Science Center, 1300 Coulter Dr, Amarillo, TX 79106, USA.

出版信息

Brain Res. 2010 Feb 2;1312:101-7. doi: 10.1016/j.brainres.2009.11.068. Epub 2009 Dec 2.

Abstract

Middle cerebral artery occlusion (MCAO) is a popular model in experimental stroke research and causes prominent ischemic damage in the forebrain. To characterize metabolic changes induced by MCAO, we have induced permanent MCAO in mice that were implanted with a microdialysis probe in either striatum or hippocampus. Immediately after the onset of ischemia, glucose levels dropped to <10% of basal values in the striatum while they dropped to 50%, and recovered thereafter, in hippocampus. Extracellular levels of glutamate rose 80-fold in the striatum but only 10-fold, and in a transient fashion, in hippocampus. In striatum, release of acetylcholine briefly increased, then dropped to very low values. Both glycerol and choline levels increased strongly during ischemia in the striatum reflecting membrane breakdown. In hippocampus, glycerol increased transiently while the increase of choline levels was moderate. Taken together, these observations delineate metabolic changes in ischemic mouse brain with the striatum representing the core area of ischemia. In comparison, the dorsal hippocampus was identified as a brain area suitable for monitoring metabolic responses in the penumbra region.

摘要

大脑中动脉阻塞(MCAO)是实验性中风研究中的一种常用模型,可导致前脑明显的缺血性损伤。为了描述 MCAO 诱导的代谢变化,我们在纹状体或海马体中植入微透析探针的小鼠中诱导永久性 MCAO。在缺血发作后,纹状体中的葡萄糖水平立即降至基础值的<10%,而在海马体中降至 50%,随后恢复。谷氨酸的细胞外水平在纹状体中升高了 80 倍,而在海马体中升高了 10 倍,且呈短暂升高。在纹状体中,乙酰胆碱的释放短暂增加,然后降至非常低的水平。在纹状体中,甘油和胆碱水平在缺血期间均强烈增加,反映了膜的破坏。在海马体中,甘油水平短暂增加,而胆碱水平的增加则适中。总的来说,这些观察结果描绘了缺血小鼠大脑中的代谢变化,纹状体代表了缺血的核心区域。相比之下,背侧海马体被确定为监测半影区代谢反应的合适脑区。

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