内分泌
词汇介绍
拓展阅读
解析
astroglial
释 义 n. 星状胶质细胞
例 句 Astroglial cells or astrocytes are specialized cells that support neuron function with nutrients and protective buffering.星形胶质细胞是一种特殊细胞,它能够通过释放营养素和缓冲保护作用支持神经元的功能。
概述
概述
星形胶质细胞是在脑和脊髓中的特性星形胶质细胞。大脑中星形胶质细胞的比例尚不明确。根据所使用的计数技术,研究发现星形胶质细胞的比例随区域而异,占所有神经胶质细胞的 20%至40%。它们执行许多功能,包括形成内皮细胞、血脑屏障,为神经组织提供营养,维持细胞外离子平衡,以及在创伤后脑和脊髓的修复和瘢痕形成过程中发挥作用。
结构
星形胶质细胞是中枢神经系统中神经胶质细胞的一种亚型,呈星形,它们的许多过程都包裹着神经元产生的突触。传统上使用组织学分析鉴定星形胶质细胞。这些细胞中的许多表达中间丝状神经胶质原纤维酸性蛋白(GFAP)。中枢神经系统中存在几种形式的星形胶质细胞,包括纤维状(白质),原生质体(灰质)。纤维神经胶质通常位于白质内,相对较少细胞器,并表现出长期无分支的细胞过程。这种类型通常具有“血管脚”,当它们靠近毛细管壁时,它们会将细胞物理连接到毛细管壁的外部。原生质胶质细胞最普遍,见于灰质组织中,具有大量的细胞器,并表现出短而高度分支的三级过程。
功能
①糖原燃料储备缓冲液:星形胶质细胞含有糖原,能够进行糖异生。额叶皮层和海马中神经元旁的星形胶质细胞储存并释放葡萄糖。因此,在高葡萄糖消耗率和葡萄糖短缺期间,星形胶质细胞可以为神经元提供葡萄糖。
②葡萄糖感测:通常与神经元有关,大脑中间质葡萄糖水平的检测也由星形胶质细胞控制。星形胶质细胞在体外被低糖激活,在体内这种激活增加了胃排空以增加消化。
③血脑屏障:围绕星形胶质细胞末端的内皮细胞被认为有助于维持血脑屏障,但最近的研究表明它们并未发挥实质性作用。相反,在维持屏障中最重要的作用是脑内皮细胞的紧密连接和基底层。但是,最近发现星形胶质细胞的活动与大脑中的血流有关,而这正是功能磁共振成像所实际测量的。
④递质的摄取和释放:星形胶质细胞表达质膜转运蛋白,例如谷氨酸转运蛋白,用于多种神经递质,包括谷氨酸,ATP和GABA。最近,显示星形胶质细胞以囊泡Ca2+依赖性方式释放谷氨酸或ATP。
⑤细胞外空间离子浓度的调节:星形胶质细胞以高密度表达钾通道。当神经元活跃时,它们会释放钾离子,从而增加局部细胞外浓度。由于星形胶质细胞对钾具有很高的渗透性,因此它们可以迅速清除细胞外空间中的过量积累。
⑥突触传递的调节:在下丘脑的视上核中,星形胶质细胞形态的快速变化已显示会影响神经元之间的异突触传递。
⑦血管调节:星形胶质细胞可以作为神经元调节血流的中介。
⑧促进少突胶质细胞的髓鞘形成活性:神经元的电活动使它们释放ATP,这是形成髓鞘的重要刺激。但是,ATP并不直接作用于少突胶质细胞。相反,它导致星形胶质细胞分泌细胞因子白血病抑制因子(LIF),一种调节蛋白,可促进少突胶质细胞的髓鞘形成活性。这表明星形胶质细胞在大脑中具有执行协调作用。
⑨神经系统修复:中枢神经系统中的神经细胞受到损伤后,星形胶质细胞会填满整个空间,形成神经胶质瘢痕,并可能有助于神经修复。
Chronic Exposure to High Altitude: Synaptic, Astroglial and Memory Changes 复制标题
高海拔慢性暴露: 突触、星形胶质细胞和记忆改变
发表时间:2019-11-11
影响指数:4.0
作者: Rupali Sharma
期刊:Sci Rep
Previous studies have shown that astrocytes have diverse functions such as establishing direct contact with neurons and secreting soluble factors at the pre-and post-synaptic sites thus modulating the structure and function of both excitatory and inhibitory synapses leading to changes in synaptic transmission. In regards to hypobaria-hypoxia, it has been shown that there is an increase in astrogliosis in the CA1 region of the hippocampus, as indicated by elevated expression of GFAP86,87. As further novelty, our findings reveal a decrease in GFAP expression in the cerebellum. It is intriguing that we observed these additional changes in the cerebellum, although at a different time point. A study by Dheer et al. studied CEHA in rats, where they observed activation of astrocytes in CA1 region of hippocampus at 7 and 14 days exposure; while Li et al., observed increased GFAP expression between 7–14 days in cortex and brainstem. The apparent discrepancy between our and their results could be due to multiple factors. One major factor is represented by the time duration, our mice in fact were exposed to a longer duration of HA, which is a chronic exposure, while their rats were exposed for a shorter period of time. Another difference is in the pressure of the hypobaric chamber, which was p=282mm/Hg (equivalent to 5.45psi) for their experiments, and ~7.4psi (equivalent to 382.69mm/Hg) for our experiments. A further difference consists in their experimental animals, which were rats while ours were mice. All these factors could have contributed to the apparent discrepancy and it is possible then that the observed decrease in GFAP, along with the decrease in other synaptic proteins, are indeed signals of decreased synaptic activity in a more generalized context of neuroplasticity occurring in response to CEHA.
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