Lapie P, Lory P, Fontaine B
INSERM CJF96108, Hôpital de la Salpêtrière, Paris, France.
Neuromuscul Disord. 1997 Jun;7(4):234-40. doi: 10.1016/s0960-8966(97)00435-5.
Hypokalemic periodic paralysis (hypoPP) is an autosomal dominant disorder characterized by acute attacks of muscle weakness concomitant to a drop in blood potassium levels. Recent molecular work has shown that hypoPP is due to mutations in a skeletal muscle voltage-gated calcium channel: the dihydropyridine receptor (DHP receptor). Mutations affect segments S4 of domains II and IV, changing an arginine in position 528 and 1239 into an histidine, or an histidine or a glycine respectively. Surprisingly, expressing in vitro mutants channels in a non-muscular environment resulted in functional calcium channels with minor modifications in electrophysiological properties. Expressing mutant channels in a muscular environment or transgenic mice might help to bridge the gap between the knowledge of the molecular defect and the understanding of the pathophysiology of the disease.
低钾性周期性麻痹(低钾型周期性麻痹,hypoPP)是一种常染色体显性疾病,其特征为伴随着血钾水平下降出现急性肌无力发作。最近的分子研究表明,低钾型周期性麻痹是由骨骼肌电压门控钙通道——二氢吡啶受体(DHP受体)的突变所致。突变影响结构域II和IV的S4片段,分别将位置528和1239处的精氨酸变为组氨酸,或将组氨酸变为甘氨酸。令人惊讶的是,在非肌肉环境中体外表达突变通道会产生功能钙通道,其电生理特性仅有微小改变。在肌肉环境中表达突变通道或构建转基因小鼠可能有助于弥合分子缺陷知识与疾病病理生理学理解之间的差距。