机译:ApoE4通过选择性地损害ApoE受体的回收利用来降低谷氨酸受体的功能和突触可塑性
Departments of Molecular Genetics Center for Alzheimer's and Neurodegenerative Disease, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046;
rnDepartments of Molecular Genetics Center for Alzheimer's and Neurodegenerative Disease, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046;
rnDepartments of Molecular Genetics Center for Alzheimer's and Neurodegenerative Disease, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046;
rnDepartments of Molecular Genetics Center for Alzheimer's and Neurodegenerative Disease, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046 Departments of Neuroscience, Center for Alzheimer's and Neurodegenerative Disease, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046;
alzheimer's disease; lipoprotein receptor; neurodegeneration; NMDA; receptor; reelin;
机译:谷氨酸受体的减少表达和CREB的磷酸化是造成体内Delta9-THC暴露受损的海马突触可塑性的原因。
机译:delta2“离子型”谷氨酸受体起非离子型受体的作用,以控制小脑突触的可塑性。
机译:寡聚淀粉样β肽在小鼠海马中对某些形式的突触可塑性的选择性损伤:突触外NMDA受体的含义
机译:谷氨酸受体通道动力学模型和2-光子激光光解分析突触传递及其可塑性
机译:Domoic acid作用机制:谷氨酸受体介导的兴奋性毒性以及海马神经传递和突触可塑性的变化。
机译:ApoE4通过选择性地损害ApoE受体的回收利用来降低谷氨酸受体的功能和突触可塑性
机译:ApoE4通过选择性地损害ApoE受体的回收利用来降低谷氨酸受体的功能和突触可塑性