Kalm Marie, Lannering Birgitta, Björk-Eriksson Thomas, Blomgren Klas
Center for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, University of Gothenburg, Box 432, SE 405 30, Sweden.
J Neuroimmunol. 2009 Jan 3;206(1-2):70-5. doi: 10.1016/j.jneuroim.2008.11.002. Epub 2008 Dec 13.
Irradiation-induced loss of neural stem and progenitor cells may contribute to cognitive deficits. Furthermore, subsequent inflammation inhibits neural progenitor cell differentiation. Here we have characterized the microglia response after a single dose of 8 Gy to the brains of postnatal day 9 or 21 rats. The number of Iba-1-positive microglia increased 6 h after IR but had decreased 7 days later, below control levels, and this decrease was more pronounced in P9 rats. Active caspase-3 and TUNEL staining revealed irradiation-induced microglia death. This age-dependent IR-induced loss of microglia likely affects both the response to IR and further brain development.
辐射诱导的神经干细胞和祖细胞损失可能导致认知缺陷。此外，随后的炎症会抑制神经祖细胞的分化。在此，我们对出生后第9天或第21天的大鼠脑部单次给予8 Gy照射后的小胶质细胞反应进行了表征。照射后6小时，Iba-1阳性小胶质细胞数量增加，但7天后减少，低于对照水平，且这种减少在出生后第9天的大鼠中更为明显。活性半胱天冬酶-3和TUNEL染色显示照射诱导小胶质细胞死亡。这种年龄依赖性的照射诱导小胶质细胞损失可能会影响对辐射的反应以及进一步的脑发育。
