Department of Physiology, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611, USA.
INSERM UMR 1195 Inserm and Universities Paris-Sud and Paris-Saclay, 80 rue du Général Leclerc, 94276 Kremlin-Bicêtre, France.
Int J Mol Sci. 2019 Jan 12;20(2):285. doi: 10.3390/ijms20020285.
Endogenous γ-aminobutyric acid (GABA)-dependent activity induces death of developing Purkinje neurons in mouse organotypic cerebellar cultures and the synthetic steroid mifepristone blocks this effect. Here, using brain-derived neurotrophic factor (BDNF) heterozygous mice, we show that BDNF plays no role in immature Purkinje cell death. However, interestingly, BDNF haploinsufficiency impairs neuronal survival induced by mifepristone and GABA-receptors antagonist (bicuculline) treatments, indicating that the underlying neuroprotective mechanism requires the neurotrophin full expression.
内源性 γ-氨基丁酸 (GABA) 依赖性活性诱导小鼠器官型小脑培养物中浦肯野神经元的死亡，而合成类固醇米非司酮可阻断此作用。在这里，我们使用脑源性神经营养因子 (BDNF) 杂合子小鼠表明 BDNF 在未成熟浦肯野细胞死亡中不起作用。然而，有趣的是，BDNF 单倍不足会损害米非司酮和 GABA 受体拮抗剂（毒蕈碱）处理诱导的神经元存活，表明潜在的神经保护机制需要神经营养因子的充分表达。
