Suppr超能文献

人中枢神经系统卫星少突胶质细胞中垂体腺苷酸环化酶激活肽(PACAP)和谷氨酸转运蛋白的表达

Expression of PACAP and glutamate transporter proteins in satellite oligodendrocytes of the human CNS.

作者信息

van Landeghem Frank K H, Weiss Thorsten, von Deimling Andreas

机构信息

Institute of Neuropathology, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany.

出版信息

Regul Pept. 2007 Jul 5;142(1-2):52-9. doi: 10.1016/j.regpep.2007.01.008. Epub 2007 Feb 6.

Abstract

White matter oligodendrocytes have been shown to actively regulate extracellular glutamate levels in the CNS. Such function has yet not been examined in satellite oligodendrocytes of gray matter. Similar to those in white matter, satellite oligodendrocytes are involved in myelination. In addition, they modulate the activity of surrounding neurons. This study examined whether satellite oligodendrocytes express PACAP and glutamate transporter proteins and whether this expression is influenced by global ischemia. We demonstrated expression of PACAP27 and PACAP38 in a major fraction of satellite oligodendrocytes in normal neocortex and hippocampus of human brain tissues obtained post-mortem. All three glutamate transporters EAAT1, EAAT2 and EAAT3 were expressed in satellite oligodendrocytes from these tissues. Thus, satellite oligodendrocytes may participate in the perineuronal glutamate homeostasis. Following transient global ischemia, the total number of satellite oligodendrocytes expressing PACAP or glutamate transporter proteins was significantly decreased in cerebral neocortex and hippocampus. However, alterations of PACAP and glutamate transporter protein expression were region and time specific. In satellite oligodendrocytes of CA1 an early strong reduction of PACAP and glutamate transporter expression was observed. This contrasted with late reduction of PACAP27, PACAP38 and glutamate transporters EAAT1, EAAT2 and EAAT3 in satellite oligodendrocytes of neocortex. Further studies should clarify whether these alterations in protein expression are primary or secondary to neuronal cell death.

摘要

白质少突胶质细胞已被证明可在中枢神经系统中积极调节细胞外谷氨酸水平。但这种功能尚未在灰质的卫星少突胶质细胞中得到研究。与白质中的少突胶质细胞类似,卫星少突胶质细胞也参与髓鞘形成。此外,它们还调节周围神经元的活性。本研究检测了卫星少突胶质细胞是否表达垂体腺苷酸环化酶激活肽(PACAP)和谷氨酸转运蛋白,以及这种表达是否受全脑缺血的影响。我们证实在死后获取的人脑组织正常新皮质和海马体中,大部分卫星少突胶质细胞表达PACAP27和PACAP38。所有三种谷氨酸转运体EAAT1、EAAT2和EAAT3均在这些组织的卫星少突胶质细胞中表达。因此,卫星少突胶质细胞可能参与神经元周围的谷氨酸稳态。短暂全脑缺血后,大脑新皮质和海马体中表达PACAP或谷氨酸转运蛋白的卫星少突胶质细胞总数显著减少。然而,PACAP和谷氨酸转运蛋白表达的改变具有区域和时间特异性。在CA1区的卫星少突胶质细胞中,观察到PACAP和谷氨酸转运蛋白表达早期显著降低。这与新皮质卫星少突胶质细胞中PACAP27、PACAP38以及谷氨酸转运体EAAT1、EAAT2和EAAT3的后期降低形成对比。进一步的研究应阐明这些蛋白质表达的改变是神经元细胞死亡的原发性还是继发性结果。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验