Department of Pharmacology & Neuroscience, Creighton University School of Medicine, Omaha, NE, USA.
Department of Pharmacology & Neuroscience, Creighton University School of Medicine, Omaha, NE, USA.
Eur J Pharmacol. 2021 Dec 15;913:174656. doi: 10.1016/j.ejphar.2021.174656. Epub 2021 Nov 25.
Drug resistant epilepsy affects ∼30% of people with epilepsy and is associated with epilepsy syndromes with frequent and multiple types of seizures, lesions or cytoarchitectural abnormalities, increased risk of mortality and comorbidities such as cognitive impairment and sleep disorders. A limitation of current preclinical models is that spontaneous seizures with comorbidities take time to induce and test, thus making them low-throughput. Kcna1-null mice exhibit all the characteristics of drug resistant epilepsy with spontaneous seizures and comorbidities occurring naturally; thus, we aimed to determine whether they also demonstrate pharmacoresistanct seizures and the impact of medications on their sleep disorder comorbidity. In this exploratory study, Kcna1-null mice were treated with one of four conventional antiseizure medications, carbamazepine, levetiracetam, phenytoin, and phenobarbital using a moderate throughput protocol (vehicle for 2 days followed by 2 days of treatment with high therapeutic doses selected based on published data in the 6 Hz model of pharmacoresistant seizures). Spontaneous recurrent seizures and vigilance states were recorded with video-EEG/EMG. Carbamazepine, levetiracetam and phenytoin had partial efficacy (67%, 75% and 33% were seizure free, respectively), whereas phenobarbital was fully efficacious and conferred seizure freedom to all mice. Thus, seizures of Kcna1-null mice appear to be resistant to three of the drugs tested. Levetiracetam failed to affect sleep architecture, carbamazepine and phenytoin had moderate effects, and phenobarbital, as predicted, restored sleep architecture. Data suggest Kcna1-null mice may be a moderate throughput model of drug resistant epilepsy useful in determining mechanisms of pharmacoresistance and testing novel therapeutic strategies.
耐药性癫痫影响约 30%的癫痫患者,与癫痫综合征相关,这些综合征常伴有多种类型的发作、病变或细胞结构异常,死亡率和合并症(如认知障碍和睡眠障碍)风险增加。目前临床前模型的一个局限性是,具有合并症的自发性癫痫需要时间来诱发和测试,因此它们的通量较低。Kcna1 基因敲除小鼠表现出所有耐药性癫痫的特征,自发性癫痫和合并症自然发生;因此,我们旨在确定它们是否也表现出耐药性癫痫发作以及药物对其睡眠障碍合并症的影响。在这项探索性研究中,Kcna1 基因敲除小鼠使用四种传统抗癫痫药物(卡马西平、左乙拉西坦、苯妥英和苯巴比妥)进行治疗,采用中等通量方案(2 天载体,然后根据发表的 6Hz 模型中耐药性癫痫发作的药物治疗数据选择高治疗剂量治疗 2 天)。使用视频-EEG/EMG 记录自发性复发性癫痫发作和警觉状态。卡马西平、左乙拉西坦和苯妥英具有部分疗效(分别有 67%、75%和 33%无癫痫发作),而苯巴比妥完全有效,使所有小鼠无癫痫发作。因此,Kcna1 基因敲除小鼠的癫痫发作似乎对三种测试药物具有耐药性。左乙拉西坦未能影响睡眠结构,卡马西平和苯妥英具有中度影响,而苯巴比妥如预期的那样恢复了睡眠结构。数据表明,Kcna1 基因敲除小鼠可能是一种中等通量的耐药性癫痫模型,可用于确定耐药机制并测试新的治疗策略。