Impairments of long-term potentiation in hippocampal slices of β-amyloid-infused rats
Impairments of long-term potentiation in hippocampal slices of β-amyloid-infused rats
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DOI：
10.1016/s0014-2999(99)00601-9
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发表时间：
1999-10-15
影响因子：
5
通讯作者：
Nabeshima, T
中科院分区：
文献类型：
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作者：
Itoh, A;Akaike, T;Nabeshima, T
在这项研究中，我们使用细胞外记录技术研究了注入 β-淀粉样蛋白（300 pmol/天，持续 10-11 天）的大鼠海马切片的神经元活动。尼古丁（50μM）的灌注降低了载体对照大鼠的CA1锥体细胞中电诱发的群体尖峰的幅度，但在注射β-淀粉样蛋白的大鼠中没有，这表明注射β-淀粉样蛋白的大鼠中烟碱信号传导受损。 CA1 锥体细胞中强直刺激诱导的长时程增强（在载体对照大鼠中很容易观察到）在注入 β-淀粉样蛋白的大鼠中也受到损害。通过向灌注溶液中添加六甲铵来阻断烟碱，抑制长时程增强诱导。综上所述，我们之前和目前的结果表明，β-淀粉样蛋白输注会损害通过烟碱乙酰胆碱受体的信号转导机制。这种功能障碍可能至少部分地导致长期增强诱导受损，并可能导致学习缺陷。 (C) 1999 Elsevier Science B.V. 保留所有权利。
In this study, we investigated the neuronal activity of hippocampal slices from the beta-amyloid protein-infused (300 pmol/day for 10-11 days) rats using the extracellular recording technique. Perfusion of nicotine (50 mu M) reduced the amplitude of electrically evoked population spikes in the CA1 pyramidal cells of the vehicle control rats, but not in those of the beta-amyloid protein-infused rats, suggesting the impairment of nicotinic signaling in the beta-amyloid protein-infused rats. Long-term potentiation induced by tetanic stimulations in CA1 pyramidal cells, which was readily observed in the vehicle control rats, was also impaired in the beta-amyloid protein-infused rats. Nicotinic blockade by adding hexamethonium into the perfused solution inhibited long-term potentiation induction. Taken together, our previous and present results suggest that beta-amyloid protein infusion impairs the signal transduction mechanisms via nicotinic acetylcholine receptors. This dysfunction may be responsible, at least in part, for the impairment of long-term potentiation induction and may lead to learning deficits. (C) 1999 Elsevier Science B.V. All rights reserved.