Jurkat-Rott Karin, Groome James, Lehmann-Horn Frank
Department of Neurophysiology, Ulm University Ulm, Germany.
Front Pharmacol. 2012 Jun 11;3:112. doi: 10.3389/fphar.2012.00112. eCollection 2012.
In voltage-gated cation channels, a recurrent pattern for mutations is the neutralization of positively charged residues in the voltage-sensing S4 transmembrane segments. These mutations cause dominant ion channelopathies affecting many tissues such as brain, heart, and skeletal muscle. Recent studies suggest that the pathogenesis of associated phenotypes is not limited to alterations in the gating of the ion-conducting alpha pore. Instead, aberrant so-called omega currents, facilitated by the movement of mutated S4 segments, also appear to contribute to symptoms. Surprisingly, these omega currents conduct cations with varying ion selectivity and are activated in either a hyperpolarized or depolarized voltage range. This review gives an overview of voltage sensor channelopathies in general and focuses on pathogenesis of skeletal muscle S4 disorders for which current knowledge is most advanced.
在电压门控阳离子通道中,突变的一个反复出现的模式是电压感应S4跨膜片段中带正电荷残基的中和。这些突变导致显性离子通道病,影响许多组织,如脑、心脏和骨骼肌。最近的研究表明,相关表型的发病机制不仅限于离子传导α孔门控的改变。相反,由突变的S4片段移动促进的异常所谓ω电流似乎也导致了症状。令人惊讶的是,这些ω电流传导具有不同离子选择性的阳离子,并在超极化或去极化电压范围内被激活。本综述概述了一般的电压传感器通道病,并重点关注骨骼肌S4疾病的发病机制,目前对此的了解最为深入。