Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, 20 Penn St, HSF-2, Baltimore, 21201 MD, USA.
Neuroscience. 2023 Feb 21;512:85-98. doi: 10.1016/j.neuroscience.2022.12.013. Epub 2022 Dec 19.
In Alzheimer's disease and related dementias, amyloid beta (Aβ) and amyloid plaques can disrupt long-term synaptic plasticity, learning and memory and cognitive function. Plaque accumulation can disrupt corticocortical circuitry leading to abnormalities in sensory, motor, and cognitive processing. In this study, using 5xFAD (five Familial Alzheimer's Disease - FAD - mutations) mice, we evaluated amyloid plaque formation in different cortical areas, and whether differential amyloid accumulation across cortical fields correlates with changes in dendritic complexity of layer 3 corticocortical projection neurons and functional responses in the primary somatosensory cortex following whisker stimulation. We focused on three cortical areas: the primary somatosensory cortex (S1), the primary motor cortex (M1), and the prefrontal cortex (PFC including the anterior cingulate, prelimbic, and infralimbic subdivisions). We found that Aβ and amyloid plaque accumulation is not uniform across 5xFAD cortical areas, while there is no expression in littermate controls. We also found that there are differential layer 3 pyramidal cell dendritic complexity changes across the three areas in 5xFAD mice, compared to same age controls, with no apparent relation to differential amyloid accumulation. We used voltage-sensitive dye imaging (VSDi) to visualize neural activity in S1, M1 and PFC following whisker activation. Control mice show normal physiological responses in all three cortical areas, whereas 5xFAD mice only display physiological responses in S1. Taken together our results show that 5xFAD mutation affects the overall dendritic morphology of layer 3 pyramidal cells across sensory-motor and association cortex irrespective of the density and distribution of the Aβ amyloid proteins. Corticocortical circuitry between the sensory and motor/association areas is most likely disrupted in 5xFAD mice as cortical responses to whisker stimulation are altered.
在阿尔茨海默病和相关痴呆症中,淀粉样蛋白β(Aβ)和淀粉样斑块可破坏长期突触可塑性、学习和记忆以及认知功能。斑块积累会破坏皮质-皮质回路,导致感觉、运动和认知处理异常。在这项研究中,我们使用 5xFAD(五种家族性阿尔茨海默病-FAD-突变)小鼠,评估了不同皮质区域的淀粉样斑块形成情况,以及皮质区域之间的淀粉样斑块积累差异是否与 3 层皮质-皮质投射神经元的树突复杂性变化以及初级体感皮层在胡须刺激后的功能反应相关。我们重点关注三个皮质区域:初级体感皮层(S1)、初级运动皮层(M1)和前额叶皮层(包括前扣带、前边缘和下边缘亚区)。我们发现 Aβ和淀粉样斑块在 5xFAD 皮质区域的积累并不均匀,而在同窝对照中没有表达。我们还发现,与同年龄的对照相比,5xFAD 小鼠在三个区域中存在 3 层锥体神经元树突复杂性的差异变化,而与淀粉样斑块的差异积累没有明显关系。我们使用电压敏感染料成像(VSDi)来可视化胡须激活后 S1、M1 和 PFC 中的神经活动。对照小鼠在所有三个皮质区域均显示出正常的生理反应,而 5xFAD 小鼠仅在 S1 中显示出生理反应。综上所述,我们的结果表明,5xFAD 突变会影响感觉-运动和联合皮层中 3 层锥体神经元的整体树突形态,而与 Aβ淀粉样蛋白的密度和分布无关。感觉和运动/联合区域之间的皮质-皮质回路很可能在 5xFAD 小鼠中受到破坏,因为胡须刺激引起的皮质反应发生了改变。