Area de Biología Celular, Instituto de Biomedicina, Universidad de León, 24071, León, Spain.
Brain Res. 2009 Sep 1;1287:20-7. doi: 10.1016/j.brainres.2009.06.065. Epub 2009 Jun 27.
Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (AMPAR) and inflammatory processes have been related to ischemia-induced damage, but there are few studies addressing their response in different brain areas. Here we compare AMPAR expression after ischemia in several brain areas (hippocampus, cerebral cortex and caudate-putamen) in an attempt to correlate it with their different vulnerabilities. We found outstanding decreases in GluR1 and GluR2 mRNA levels after global ischemia and 48 h reperfusion (I/R) in all the areas studied, however, protein levels maintained in some areas such as CA3, suggesting different post-transcriptional control in different areas of the brain. To characterize the inflammatory response in these areas, we measured the mRNA levels of CD11b/CD18 membrane integrin (a reactive microglia marker), which showed an important but similar up-regulation in all brain areas studied, which was confirmed by immunohistochemistry. We conclude that the down-regulation of AMPAR gene expression following I/R does not explain differences in the vulnerability of different areas. Additionally, our data indicate that the level of inflammation is independent of the vulnerability of the different brain areas and does not explain differences in the AMPAR expression observed in the brain areas studied.
α-氨基-3-羟基-5-甲基异恶唑-4-丙酸受体（AMPAR）和炎症过程与缺血诱导的损伤有关，但关于它们在不同脑区的反应的研究较少。在这里，我们比较了缺血后不同脑区（海马体、大脑皮层和尾状核-壳核）的 AMPAR 表达，试图将其与它们不同的脆弱性相关联。我们发现，在所有研究的区域中，在全脑缺血和 48 小时再灌注（I/R）后，GluR1 和 GluR2 mRNA 水平明显下降，但在 CA3 等一些区域，蛋白质水平保持不变，表明不同脑区存在不同的转录后控制。为了表征这些区域的炎症反应，我们测量了 CD11b/CD18 膜整合素（一种反应性小胶质细胞标志物）的 mRNA 水平，结果显示所有研究区域的表达均显著上调，免疫组织化学证实了这一点。我们得出结论，I/R 后 AMPAR 基因表达的下调并不能解释不同区域易损性的差异。此外，我们的数据表明，炎症水平与不同脑区的易损性无关，也不能解释在研究的脑区中观察到的 AMPAR 表达的差异。
