Mechanism underlying the glucocorticoid-decreased function of neurotrophic factor in depression.

抑郁症中糖皮质激素降低神经营养因子功能的机制。

• 批准号: 21680034
• 负责人: NUMAKAWA Tadahiro
• 金额: $ 16.81万
• 依托单位: National Center of Neurology and Psychiatry
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (A)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21680034/
• 关键词: 精神; 神経疾患の病態と治療; 神経科学; 脳神経疾患; 細胞・組織; 精神; 神経疾患の病態と治療; 神経科学; 脳神経疾患; 細胞・組織

Following glucocorticoid(stress hormone) exposure, BDNF-dependent synaptic maturation was decreased in cultured cortical neurons. We found that shp2-TrkB interaction, which is important for BDNF-mediated synaptic protein expression, was also reduced. In vivo models, we examined possible change of BDNF-related intracellular signaling in forebrain after restraint stress. We found that significant GR downregulation after restraint operation and confirmed a decrease in BDNF-stimulated neurotransmitter release.

糖皮质激素（应激激素）暴露后，培养的皮质神经元中依赖BDNF的突触成熟。我们发现SHP2-TRKB相互作用对BDNF介导的突触蛋白表达很重要，也降低了。在体内模型中，我们检查了约束应力后前脑中BDNF相关的细胞内信号传导的可能变化。我们发现，约束操作后明显的GR下调，并证实了BDNF刺激的神经递质释放的降低。