Acarin L, González B, Hidalgo J, Castro A J, Castellano B
Department of Cell Biology and Physiology, Autonomous University of Barcelona, Bellaterra, Spain.
Neuroscience. 1999;92(3):827-39. doi: 10.1016/s0306-4522(99)00022-6.
In this study we have evaluated the primary astroglial reactivity to an injection of N-methyl-D-aspartate into the right sensorimotor cortex, as well as the secondary astroglial response in the thalamic ventrobasal complex, caused by the anterograde degeneration of descending corticothalamic fibres and/or target deprivation of the developing thalamic neurons. The astroglial response was evaluated from 4 h to 30 days post-lesion, by the immunocytochemical detection of the cytoskeletal proteins glial fibrillary acidic protein and vimentin, and the antioxidant and metal binding protein metallothionein I-II. In the lesioned cortex, hypertrophied reactive astrocytes showed increased glial fibrillary acidic protein labelling that correlated with a strong expression of vimentin and metallothionein I-II. Maximal astrocytic response was seen at one week post-lesion. The glial scar that formed later on remained positive for all astroglial markers until the last survival time examined. In contrast, in the anterogradely/retrogradely affected thalamus, the induced astroglial secondary response was not as prominent as in the cortex and was characteristically transitory, being undetectable by 14 days post-lesion. Interestingly, thalamic reactive astrocytes showed increased glial fibrillary acidic protein expression but no induction of vimentin and metallothionein I-II. In conclusion, in the young brain, the pattern of astroglial reactivity is not homogeneous and is strongly dependent on the grade of tissue damage: both in response to primary neuronal death and in response to retrograde/anterograde secondary damage, reactive astrocytes show hypertrophy and increased glial fibrillary acidic protein expression. However, astroglial vimentin and metallothionein I-II expression are only observed in areas undergoing massive neuronal death, where glial scar is formed.
在本研究中，我们评估了原发性星形胶质细胞对向右侧感觉运动皮层注射N-甲基-D-天冬氨酸的反应，以及丘脑腹侧基底复合体中的继发性星形胶质细胞反应，该反应由下行皮质丘脑纤维的顺行性变性和/或发育中的丘脑神经元的靶剥夺引起。在损伤后4小时至30天，通过免疫细胞化学检测细胞骨架蛋白胶质纤维酸性蛋白和波形蛋白，以及抗氧化和金属结合蛋白金属硫蛋白I-II，评估星形胶质细胞反应。在受损皮层中，肥大的反应性星形胶质细胞显示胶质纤维酸性蛋白标记增加，这与波形蛋白和金属硫蛋白I-II的强烈表达相关。在损伤后一周观察到最大的星形胶质细胞反应。后来形成的胶质瘢痕在所有星形胶质细胞标记物上均保持阳性，直至检查的最后存活时间。相比之下，在顺行性/逆行性受影响的丘脑中，诱导的星形胶质细胞继发性反应不如皮层中明显，并且具有典型的短暂性，在损伤后14天无法检测到。有趣的是，丘脑反应性星形胶质细胞显示胶质纤维酸性蛋白表达增加，但波形蛋白和金属硫蛋白I-II未诱导表达。总之，在幼龄脑中，星形胶质细胞反应模式并不均匀，并且强烈依赖于组织损伤程度：无论是对原发性神经元死亡的反应还是对逆行性/顺行性继发性损伤的反应，反应性星形胶质细胞均显示肥大和胶质纤维酸性蛋白表达增加。然而，仅在发生大量神经元死亡并形成胶质瘢痕的区域观察到星形胶质细胞波形蛋白和金属硫蛋白I-II表达。
