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CA1 海马锥体神经元在斑块前 CRND8 小鼠中的生理学变化。

Changes in the physiology of CA1 hippocampal pyramidal neurons in preplaque CRND8 mice.

机构信息

Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

出版信息

Neurobiol Aging. 2012 Aug;33(8):1609-23. doi: 10.1016/j.neurobiolaging.2011.05.001. Epub 2011 Jun 15.

DOI:10.1016/j.neurobiolaging.2011.05.001
PMID:21676499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3175257/
Abstract

Amyloid-β protein (Aβ) is thought to play a central pathogenic role in Alzheimer's disease. Aβ can impair synaptic transmission, but little is known about the effects of Aβ on intrinsic cellular properties. Here we compared the cellular properties of CA1 hippocampal pyramidal neurons in acute slices from preplaque transgenic (Tg+) CRND8 mice and wild-type (Tg-) littermates. CA1 pyramidal neurons from Tg+ mice had narrower action potentials with faster decays than neurons from Tg- littermates. Action potential-evoked intracellular Ca(2+) transients in the apical dendrite were smaller in Tg+ than in Tg- neurons. Resting calcium concentration was higher in Tg+ than in Tg- neurons. The difference in action potential waveform was eliminated by low concentrations of tetraethylammonium ions and of 4-aminopyridine, implicating a fast delayed-rectifier potassium current. Consistent with this suggestion, there was a small increase in immunoreactivity for Kv3.1b in stratum radiatum in Tg+ mice. These changes in intrinsic properties may affect information flow through the hippocampus and contribute to the behavioral deficits observed in mouse models and patients with early-stage Alzheimer's disease.

摘要

淀粉样β蛋白（Aβ）被认为在阿尔茨海默病的发病机制中起核心作用。Aβ 可损害突触传递，但对于 Aβ 对固有细胞特性的影响知之甚少。在这里，我们比较了早发性斑块转基因（Tg+）CRND8 小鼠和野生型（Tg-）同窝仔鼠急性脑片中 CA1 海马锥体神经元的细胞特性。与 Tg-仔鼠神经元相比，Tg+仔鼠的 CA1 锥体神经元的动作电位更窄，衰减更快。与 Tg-神经元相比，Tg+神经元的树突顶端动作电位诱发的细胞内 Ca（2+）瞬变更小。Tg+神经元中的静息钙浓度高于 Tg-神经元。动作电位波形的差异被低浓度的四乙铵离子和 4-氨基吡啶消除，表明存在快速延迟整流钾电流。与这一假设一致，在 Tg+仔鼠的放射状层中 Kv3.1b 的免疫反应性略有增加。这些内在特性的变化可能会影响通过海马的信息流，并导致在阿尔茨海默病早期阶段的小鼠模型和患者中观察到的行为缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/b6b991c4e15d/nihms-296353-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/a6b7e0984445/nihms-296353-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/70df73c0bb12/nihms-296353-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/ab2c270336ee/nihms-296353-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/1373875b69ee/nihms-296353-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/b324c842d67c/nihms-296353-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/5092902501ed/nihms-296353-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/b6b991c4e15d/nihms-296353-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/a6b7e0984445/nihms-296353-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/70df73c0bb12/nihms-296353-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/ab2c270336ee/nihms-296353-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/1373875b69ee/nihms-296353-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/b324c842d67c/nihms-296353-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/5092902501ed/nihms-296353-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f5d/3175257/b6b991c4e15d/nihms-296353-f0007.jpg

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