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首页> 外文期刊>Neuron >Fleeting activation of ionotropic glutamate receptors sensitizes cortical neurons to complement attack.
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Fleeting activation of ionotropic glutamate receptors sensitizes cortical neurons to complement attack.

机译：离子型谷氨酸受体的短暂激活会激活皮层神经元以补充攻击。

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Insidious attack of cortical neurons by complement has been implicated in Alzheimer's and other neurodegenerative diseases. Excitotoxicity, triggered by excessive activation of glutamate receptors, has been implicated in neuronal death following diverse insults, including ischemia and seizures. Clinical studies suggested that a minimal excitotoxic insult might sensitize neurons to complement attack. We found that fleeting activation of ionotropic glutamate receptors sensitizes neurons but not astrocytes to complement attack. The complement molecule effecting cytotoxicity was the membrane attack complex. The site within the complement cascade at which sensitization was effected was the membrane attack pathway. Sensitization mediated by glutamate receptor activation required Ca(2+)(o) and generation of reactive oxygen species. These in vitro findings predict that a fleeting excitotoxic insult could act synergistically with complement to destroy cortical neurons and accelerate neurological deterioration.
机译：补体对皮质神经元的隐性攻击已经牵涉到阿尔茨海默氏病和其他神经退行性疾病。由谷氨酸受体的过度活化引发的兴奋性毒性，已牵涉到多种损伤（包括缺血和癫痫发作）后的神经元死亡。临床研究表明，最小程度的兴奋性毒性损伤可能会使神经元敏感，以补充攻击。我们发现，离子型谷氨酸受体的短暂激活会激活神经元而不是星形胶质细胞来补充攻击。影响细胞毒性的补体分子是膜攻击复合物。补体级联内发生敏化的位点是膜攻击途径。谷氨酸受体激活介导的敏化需要Ca（2 +）（o）和活性氧的生成。这些体外发现预示着短暂的兴奋性毒性损伤可能与补体协同作用，破坏皮层神经元并加速神经系统恶化。

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