Effect of β-amyloid peptide on behavior and synaptic plasticity in terrestrial snail
Effect of β-amyloid peptide on behavior and synaptic plasticity in terrestrial snail
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DOI：
10.1016/j.brainresbull.2005.05.023
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发表时间：
2005-09-30
影响因子：
3.8
通讯作者：
Balaban, PM
中科院分区：
文献类型：
--
作者：
Samarova, EI;Bravarenko, NI;Balaban, PM
大量证据表明，β-淀粉样肽 (β AP) 和进化上高度保守的淀粉样前体蛋白 (APP) 的其他衍生物与阿尔茨海默病的发病机制有关。然而。 APP 及其蛋白水解衍生物与突触可塑性的功能关系尚不清楚。我们证明，暴露于 25-35 β AP 片段 30 分钟不会显着改变已识别的陆生蜗牛神经元中突触反应的动态，而应用 180 分钟 β AP 浴后观察到长期敏化显着降低。在行为实验中，敏化显着降低。注射βAP后观察到厌恶食物条件反射的能力下降。我们的结果清楚地表明，βAP 的神经毒性 25-35 片段可能通过长期消除某些潜在形式的突触可塑性，在行为可塑性中发挥重要作用。该研究还提出了一种新的阿尔茨海默病无脊椎动物模型。 (c) 2005 Elsevier Inc. 保留所有权利。
A large body of evidence implicates beta-amyloid peptide (beta AP) and other derivatives of the evolutionarily highly conserved amyloid precursor protein (APP) in the pathogenesis of Alzheimer's disease. However. the functional relationship of APP and its proteolytic derivatives to synaptic plasticity is not well known. We demonstrate that 30 min exposure to the 25-35 fragment of beta AP do not markedly change the dynamics of synaptic responses in identified neurons of terrestrial snail while a significant decrease of long-term sensitization was observed after 180 min beta AP bath application. In the behavioral experiments, a significant reduction of sensitization. and decreased ability to develop food-aversion conditioning was observed after beta AP injection. Our results clearly demonstrate that the neurotoxic 25-35 fragment of beta AP may play a significant role in behavioral plasticity by chronically eliminating certain underlying forms of synaptic plasticity, The study also proposes a novel invertebrate model to Alzheimer's disease. (c) 2005 Elsevier Inc. All rights reserved.