Biological Psychiatry·· 2 天前AI 评分22
脆性X综合征模型中GluN2D NMDA受体的细胞类型特异性转换驱动皮层环路过度兴奋与感觉驱动同步缺陷
A cell type-specific switch in GluN2D NMDA receptors drives cortical circuit hyperexcitability and sensory-driven cortical synchronization deficits in a Fragile X Syndrome model
AI 导读
脆性X综合征模型中发现，GluN2D NMDA受体发生细胞类型特异性转换，驱动皮层环路过度兴奋及感觉驱动的皮层同步缺陷。该研究发表于Biological Psychiatry，由Aleya Shedd等开展，提示GluN2D可能是脆性X综合征皮层功能障碍的潜在靶点。
来源：Biological Psychiatry · sciencedirect.com