Effects of Aβ exposure on long-term associative memory and its neuronal mechanisms in a defined neuronal network.
Effects of Aβ exposure on long-term associative memory and its neuronal mechanisms in a defined neuronal network.
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DOI：
10.1038/srep10614
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发表时间：
2015-05-29
影响因子：
4.6
通讯作者：
Kemenes G
中科院分区：
文献类型：
--
作者：
Ford L;Crossley M;Williams T;Thorpe JR;Serpell LC;Kemenes G
β淀粉样蛋白（Aβ）诱导的神经元死亡与记忆丧失有关，这可能是阿尔茨海默病（AD）最具破坏性的症状。虽然已知a β诱导的突触或内在可塑性损伤发生在任何细胞死亡之前，但这些神经生理变化与特定类型行为记忆丧失之间的联系尚未完全了解。在这里，我们使用行为和生理上易于处理的动物模型来研究在没有神经元死亡的情况下，a β诱导的记忆丧失和电生理变化。我们发现Aβ 25-35和Aβ 1-42在蜗牛的进食回路中有相似的行为作用，但有不同的神经生理作用。重要的是，我们还确定了行为和神经元效应都依赖于动物在治疗前的经典条件反射，因为在训练前应用a β不会导致记忆障碍，也不会在治疗后的相当时间内引起潜在的神经元变化。
Amyloid beta (Aβ) induced neuronal death has been linked to memory loss, perhaps the most devastating symptom of Alzheimer’s disease (AD). Although Aβ-induced impairment of synaptic or intrinsic plasticity is known to occur before any cell death, the links between these neurophysiological changes and the loss of specific types of behavioral memory are not fully understood. Here we used a behaviorally and physiologically tractable animal model to investigate Aβ-induced memory loss and electrophysiological changes in the absence of neuronal death in a defined network underlying associative memory. We found similar behavioral but different neurophysiological effects for Aβ 25-35 and Aβ 1-42 in the feeding circuitry of the snail Lymnaea stagnalis. Importantly, we also established that both the behavioral and neuronal effects were dependent upon the animals having been classically conditioned prior to treatment, since Aβ application before training caused neither memory impairment nor underlying neuronal changes over a comparable period of time following treatment.
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