Tong L, Perez-Polo R
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77555-0652, USA.
J Neural Transm (Vienna). 1998;105(8-9):905-14. doi: 10.1007/s007020050101.
In the present study, cell death induced by glucose deprivation in primary cultures of cerebellar granule neurons was examined. Glucose deprivation-induced apoptotic cell death was demonstrated using the terminal transferase-mediated (TdT) deoxyuridine triphosphate (d-UTP)-biotin nick end labeling (TUNEL) method and DNA fragmentation assays. When the effects of different neurotrophins on the survival of cerebellar granule neurons after glucose deprivation were assessed, BDNF, but not NT-3 or NGF, was found to protect cerebellar granule neurons against glucose deprivation-induced cell death. In addition, BDNF treatment increased c-Fos immunoreactivity in the cerebellar granule neurons. These results are consistent with the hypothesis that neuronal death due to glucose deprivation has a significant apoptotic component and that neurotrophins can protect against hypoglycemic damage.
在本研究中，检测了原代培养的小脑颗粒神经元中葡萄糖剥夺诱导的细胞死亡。使用末端转移酶介导的（TdT）脱氧尿苷三磷酸（d-UTP）-生物素缺口末端标记（TUNEL）法和DNA片段化分析证实了葡萄糖剥夺诱导的凋亡性细胞死亡。当评估不同神经营养因子对葡萄糖剥夺后小脑颗粒神经元存活的影响时，发现脑源性神经营养因子（BDNF）而非神经营养因子-3（NT-3）或神经生长因子（NGF）可保护小脑颗粒神经元免受葡萄糖剥夺诱导的细胞死亡。此外，BDNF处理增加了小脑颗粒神经元中c-Fos免疫反应性。这些结果与以下假设一致，即由于葡萄糖剥夺导致的神经元死亡具有显著的凋亡成分，并且神经营养因子可以防止低血糖损伤。
