Haupt C, Witte O W, Frahm C
Department of Neurology, Friedrich-Schiller-University, Erlanger Allee 101, 07747 Jena, Germany.
Neuroscience. 2007 Jan 19;144(2):562-70. doi: 10.1016/j.neuroscience.2006.09.054. Epub 2006 Nov 15.
Following focal ischemic injury, several mechanisms lead to secondary expansion of the affected area and therefore increase the initial damage. We thoroughly investigated the expression of astrocytic connexin 43 (Cx43) after photothrombosis in rat brain. The temporal profile of Cx43 mRNA as well as protein expression was studied in remote, structurally uninjured cortical and hippocampal areas. The hippocampal formation revealed an increased number of Cx43 mRNA positive astrocytes and an up-regulated protein expression exclusively in the ipsilateral stratum oriens. We assume a participation of this region in glia scar formation. While Cx43 mRNA positive cells were transiently increased, immunoreactivity was reduced in the somatosensory cortex of injured hemispheres. The observed decrease of Cx43 protein in the post-ischemic cerebral cortex implies an impairment of gap junctional intercellular communication which might be detrimental to the brain.
局灶性缺血性损伤后，多种机制会导致受影响区域的继发性扩展，从而增加初始损伤。我们深入研究了大鼠脑光血栓形成后星形胶质细胞连接蛋白43（Cx43）的表达。在结构未受损的远隔皮质和海马区域研究了Cx43 mRNA以及蛋白质表达的时间变化情况。海马结构显示，仅在同侧的海马下托中，Cx43 mRNA阳性星形胶质细胞数量增加且蛋白质表达上调。我们推测该区域参与了胶质瘢痕形成。虽然Cx43 mRNA阳性细胞短暂增加，但在损伤半球的体感皮层中免疫反应性降低。在缺血后大脑皮层中观察到的Cx43蛋白减少意味着间隙连接细胞间通讯受损，这可能对大脑有害。
