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首页> 外文期刊>Neuron >Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease.
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Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease.

机译：阿尔茨海默氏病小鼠模型中异常兴奋性神经元活动和抑制性海马回路的补偿性重塑。

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Neural network dysfunction may play an important role in Alzheimer's disease (AD). Neuronal circuits vulnerable to AD are also affected in human amyloid precursor protein (hAPP) transgenic mice. hAPP mice with high levels of amyloid-beta peptides in the brain develop AD-like abnormalities, including cognitive deficits and depletions of calcium-related proteins in the dentate gyrus, a region critically involved in learning and memory. Here, we report that hAPP mice have spontaneous nonconvulsive seizure activity in cortical and hippocampal networks, which is associated with GABAergic sprouting, enhanced synaptic inhibition, and synaptic plasticity deficits in the dentate gyrus. Many Abeta-induced neuronal alterations could be simulated in nontransgenic mice by excitotoxin challenge and prevented in hAPP mice by blocking overexcitation. Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD.
机译：神经网络功能障碍可能在阿尔茨海默氏病（AD）中起重要作用。易患AD的神经元回路在人类淀粉样蛋白前体蛋白（hAPP）转基因小鼠中也受到影响。在大脑中具有高淀粉样β肽水平的hAPP小鼠会出现AD样异常，包括认知缺陷和齿状回中钙相关蛋白的消耗，齿状回是关键参与学习和记忆的区域。在这里，我们报告hAPP小鼠在皮质和海马网络中具有自发的非惊厥性癫痫发作活动，这与GABA能发芽，增强的突触抑制和齿状回的突触可塑性缺陷有关。通过兴奋性毒素攻击，可以在非转基因小鼠中模拟许多Abeta诱导的神经元改变，并通过阻止过度兴奋在hAPP小鼠中防止这种改变。海马中网络兴奋性和代偿性抑制机制的异常增加可能导致hAPP小鼠以及可能患有AD的人中Abeta诱导的神经功能缺损。

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