Bordey A, Hablitz J J, Sontheimer H
Department of Neurobiology, University of Alabama at Birmingham, 35294, USA.
Neuroreport. 2000 Sep 28;11(14):3151-5. doi: 10.1097/00001756-200009280-00022.
Injury and diseases of the nervous system can induce astrocytes to form tenacious glial scars. We induced focal cortical freeze-lesions in neonatal rats and examined scars histologically and electrophysiologically in tissue slices isolated 2-3 weeks after lesioning. Lesions displayed marked gliosis, characterized by upregulation of GFAP labeling. Reactive astrocytes surrounding the scar showed marked hypertrophy, enlarged cell bodies and extended processes frequently terminating with endfeet-like structures on blood vessels. These reactive astrocytes showed enhanced expression of inwardly rectifying K+ (K(IR)) channels, widely believed to be an important pathway for astrocytic K+ buffering. These results suggest that a subpopulation of reactive astrocytes along a glial scar might be instrumental in buffering K+ away from the lesion.
神经系统的损伤和疾病可诱导星形胶质细胞形成坚韧的胶质瘢痕。我们在新生大鼠中诱导局灶性皮质冷冻损伤，并在损伤后2-3周分离的组织切片中对瘢痕进行组织学和电生理学检查。损伤显示出明显的胶质增生，其特征是GFAP标记上调。瘢痕周围的反应性星形胶质细胞表现出明显的肥大，细胞体增大，突起延长，常常在血管上以终足样结构终止。这些反应性星形胶质细胞显示内向整流钾（K(IR)）通道的表达增强，人们普遍认为这是星形胶质细胞缓冲钾离子的重要途径。这些结果表明，沿着胶质瘢痕的反应性星形胶质细胞亚群可能有助于将钾离子从损伤部位缓冲出去。
