A number of hypotheses have been put forward as to why humans respond to fever by seizing. The current leading hypotheses are that respiratory alkalosis produces an as yet unidentified change in neural excitability or that inflammatory mediators potentiate excitatory synaptic transmission. However, it is well known that ion channel gating rates increase with increased temperature. Furthermore, skeletal and cardiac sodium channel activation can be temperature sensitive in some situations. We measured the temperature sensitivity of the brain sodium channel, NaV1.2, to determine whether febrile temperatures might produce a direct increase in neuronal excitability.

中文翻译：

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热打开轴突起始段钠通道：热性惊厥机制？

已经提出了许多关于为什么人类通过抓住来对发烧做出反应的假设。目前的主要假设是呼吸性碱中毒导致神经兴奋性发生尚未确定的变化，或者炎症介质增强兴奋性突触传递。然而，众所周知，离子通道门控率随温度升高而增加。此外，骨骼和心脏钠通道激活在某些情况下可能对温度敏感。我们测量了脑钠通道 NaV1.2 的温度敏感性，以确定发热温度是否会直接增加神经元兴奋性。