Stroke-induced changes in neuroglia determine the basic conditions for the survival and damage of neurons in the ischemic core. Here, we studied the immunolocalization of glial cell line-derived neurotrophic factor (GDNF), glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor molecule 1 (Iba-1), and S-100β in the rat parietal cortex after constant occlusion of the middle cerebral artery. These cytoplasmic proteins are specific for different glial cell types. They are used as indicators of activated microglia and astrocytes in immunocytochemical studies.

The distribution pattern of all markers changed dramatically with time. GFAP- and S-100β-positive astrocytes were observed in the penumbra zone and marked its boundaries. In days 1–8 after surgery, in the ischemic core, the number of S-100β-immunoreactive astrocytes decreased, and individual pyramidal cells appeared. S-100β-expressing pyramidal cells were localized in cortical layers III and V. They were only found in the ischemic core. Their proportion to the total number of cells was 37.3 ± 3.9 %, 22.2 ± 1.2 %, 16.3 ± 2.3 %, and 5.4 ± 0.3 % on days 1, 3, 8, and 14 after surgery. On day 21, no S-100β-expressing pyramidal cells were observed. The spatial density of GFAP- and S-100β-positive astrocytes increased in the penumbra region adjacent to the ischemic core and decreased in the penumbral periphery. As a result, the width of the perifocal penumbra zone decreased substantially at later stages of the stroke. In the penumbra, on days 1–3 after ischemic injury, GDNF immunoreactivity was mainly localized in neurons, while later on (days 8–21) it was mainly constrained to astrocyte glia. In intact rats, GDNF-positive neurons were situated in cortical layers II/III and V/VI and made up 52 ± 4.5 % of the total neuron population. Their proportion to the total number of neurons was 29 ± 2.1 %, 13.8 ± 0.6 %, and 3.1 ± 0.2 % on days 1, 8, and 21 after surgery. The number of GDNF-positive astrocytes, on the opposite, increased with time after ischemic injury. Iba-1-reactive microglia was mainly localized to the ischemic core. Microglial cells appeared activated as evidenced by their increased size and decreased number of processes and branching density. The spatial density of microglia reached a peak ​​on day 8 after ischemic injury both in the ischemic core and penumbra. An increase in the number of Iba-1-reactive microglia in the ischemic core correlated with a decrease of the number of GFAP-positive astrocytes. The results are discussed in the context of participation of neuroglia in regulation of various neuroprotective and destructive processes.

中风引起的神经胶质细胞变化决定了缺血核心神经元存活和损伤的基本条件。在这里，我们研究了恒定时间后大鼠顶叶皮质中神经胶质细胞源性神经营养因子（GDNF），神经胶质原纤维酸性蛋白（GFAP），钙离子结合适配器分子1（Iba-1）和S-100β的免疫定位阻塞大脑中动脉。这些细胞质蛋白对不同的胶质细胞类型具有特异性。它们在免疫细胞化学研究中用作活化的小胶质细胞和星形胶质细胞的指标。

所有标记的分布模式都随时间发生了巨大变化。在半影区观察到了GFAP和S-100β阳性星形胶质细胞，并标记了其边界。术后1-8天，在缺血核心，S-100β免疫反应性星形胶质细胞数量减少，并出现单个锥体细胞。表达S-100β的锥体细胞位于皮质层III和V中。它们仅在缺血核心中发现。在手术后第1、3、8和14天，它们在细胞总数中所占的比例分别为37.3±3.9％，22.2±1.2％，16.3±2.3％和5.4±0.3％。在第21天，未观察到表达S-100β的锥体细胞。GFAP和S-100β阳性星形胶质细胞的空间密度在邻近缺血核心的半影区域增加，而在半影周围减少。结果是，在卒中的后期阶段，局灶性半影区的宽度明显减小。在半影中，在缺血性损伤后的第1-3天，GDNF的免疫反应性主要集中在神经元中，而随后（第8-21天），它主要局限于星形胶质细胞的胶质细胞。在完整的大鼠中，GDNF阳性神经元位于皮层II / III和V / VI中，占总神经元群体的52±4.5％。在术后第1、8和21天，它们在神经元总数中所占的比例为29±2.1％，13.8±0.6％和3.1±0.2％。相反，缺血性损伤后，GDNF阳性星形胶质细胞的数量随时间增加。Iba-1反应性小胶质细胞主要位于缺血核心。小胶质细胞的大小增加，过程数量和分支密度降低证明其被激活。小脑胶质瘤的空间密度在缺血损伤后第8天在缺血核心和半影处达到峰值。缺血核心中Iba-1反应性小胶质细胞数量的增加与GFAP阳性星形胶质细胞数量的减少有关。在神经胶质参与各种神经保护和破坏过程的调节的背景下讨论了结果。