长时程增强
NMDA受体
海马体
神经科学
心理学
受体
医学
内科学
作者
Nicolina Südkamp,Olena Shchyglo,Denise Manahan‐Vaughan
标识
DOI:10.3389/fnagi.2024.1377085
摘要
Studies in rodent models have revealed that oligomeric beta-amyloid protein [Aβ (1-42)] plays an important role in the pathogenesis of Alzheimer's disease. Early elevations in hippocampal neuronal excitability caused by Aβ (1-42) have been proposed to be mediated via enhanced activation of GluN2B-containing N-methyl-D-aspartate receptors (NMDAR). To what extent GluN2A or GluN2B-containing NMDAR contribute to Aβ (1-42)-mediated impairments of hippocampal function in advanced rodent age is unclear. Here, we assessed hippocampal long-term potentiation (LTP) and neuronal responses 4-5 weeks after bilateral intracerebral inoculation of 8-15 month old GluN2A
科研通智能强力驱动
Strongly Powered by AbleSci AI