Respiratory alkalosis provokes spike-wave discharges in seizure-prone rats.
Respiratory alkalosis provokes spike-wave discharges in seizure-prone rats.
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DOI：
10.7554/elife.72898
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发表时间：
2022-01-04
期刊：
影响因子：
7.7
通讯作者：
Beenhakker MP
中科院分区：
文献类型：
--
作者：
Salvati KA;Souza GMPR;Lu AC;Ritger ML;Guyenet P;Abbott SB;Beenhakker MP
在诊断为缺乏性癫痫的患者中，过度通气确实会引起癫痫发作。尽管有这种可预测的患者反应，但使过度通气强有力地激活癫痫发作回路的机制仍然完全未知。通过在WAG/Rij大鼠（一种已建立的失神癫痫啮齿动物模型）中使用气体交换操作和光遗传学，我们发现失神癫痫对动脉二氧化碳高度敏感，这表明癫痫发生回路对ph敏感。此外，过度通气持续激活丘脑层间核内的神经元，这一结构与癫痫发生有关。我们发现，丘脑层内也含有ph敏感神经元。总的来说，这些观察结果表明，过度通气激活板间核的ph敏感神经元，引起失神发作。
Hyperventilation reliably provokes seizures in patients diagnosed with absence epilepsy. Despite this predictable patient response, the mechanisms that enable hyperventilation to powerfully activate absence seizure-generating circuits remain entirely unknown. By utilizing gas exchange manipulations and optogenetics in the WAG/Rij rat, an established rodent model of absence epilepsy, we demonstrate that absence seizures are highly sensitive to arterial carbon dioxide, suggesting that seizure-generating circuits are sensitive to pH. Moreover, hyperventilation consistently activated neurons within the intralaminar nuclei of the thalamus, a structure implicated in seizure generation. We show that intralaminar thalamus also contains pH-sensitive neurons. Collectively, these observations suggest that hyperventilation activates pH-sensitive neurons of the intralaminar nuclei to provoke absence seizures.