体外诱导的神经元活动不会减弱淀粉样β蛋白诱导的突触损失。
Induced neuronal activity does not attenuate amyloid beta-induced synaptic loss in vitro.
作者信息
Kono Rena, Kim Gyu Li, Nagata Hidetaka, Ikegaya Yuji, Koyama Ryuta
机构信息
Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Platform Technology Research Unit, Sumitomo Dainippon Pharma Co., Ltd., Osaka, Japan.
出版信息
Neuropsychopharmacol Rep. 2019 Dec;39(4):306-311. doi: 10.1002/npr2.12074. Epub 2019 Aug 3.
AIM
The accumulation of amyloid beta (Aβ) is one of the characteristics of Alzheimer's disease. The excessive accumulation of Aβ has been suggested to result in a decrease in the number of synapses. Although the number of synapses is generally modulated by neuronal activity, whether neuronal activity affects Aβ-induced synapse loss remains unknown. Therefore, we addressed this question using a primary culture of hippocampal neurons.
METHOD
The neuronal activity of cultured hippocampal neurons from mouse pups was increased using the chemogenetic technique designer receptors exclusively activated by designer drugs (DREADD). The cultured neurons were treated with Aβ, and synapse density was assessed by immunocytochemistry.
RESULTS
Aβ decreased the synapse density probably by decreasing postsynapse. On the other hand, enhanced neuronal activity did not affect the synapse density significantly. However, there was a trend that enhanced neuronal activity increased especially presynapse density.
CONCLUSION
We found that enhanced neuronal activity did not affect Aβ-induced synapse loss in vitro.
目的
β-淀粉样蛋白（Aβ）的积累是阿尔茨海默病的特征之一。有人提出，Aβ的过度积累会导致突触数量减少。虽然突触数量通常受神经元活动调节，但神经元活动是否会影响Aβ诱导的突触损失仍不清楚。因此，我们使用海马神经元原代培养来解决这个问题。
方法
利用仅由设计药物激活的化学遗传技术（DREADD）提高来自幼鼠的培养海马神经元的神经元活性。用Aβ处理培养的神经元，并通过免疫细胞化学评估突触密度。
结果
Aβ可能通过减少突触后成分降低突触密度。另一方面，增强的神经元活动对突触密度没有显著影响。然而，有一个趋势是增强的神经元活动尤其增加了突触前密度。
结论
我们发现在体外增强的神经元活动不影响Aβ诱导的突触损失。
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