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Effects of Na+ channel isoforms and lipid membrane environment on temperature tolerance of cardiac Na+ current in zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss)
bioRxiv - Physiology Pub Date : 2020-11-20 , DOI: 10.1101/2020.11.20.391334
Jaakko Haverinen , Irina Dzhumaniiazova , Denis V. Abramochkin , Minna Hassinen , Matti Vornanen

Heat tolerance of heart rate in fish is suggested to be limited by impaired electrical excitation of the ventricle due to the antagonistic effects of high temperature on Na+ (INa) and K+ (IK1) ion currents (INa is depressed at high temperatures while IK1 is resistant to them). To examine the role of Na+ channel proteins and the lipid matrix of the channels in heat tolerance of INa, we compared temperature-dependencies of zebrafish (Danio rerio) and rainbow trout (Oncorhynchus mykiss) ventricular INa, and INa generated by the cloned zebrafish and rainbow trout NaV1.4 and NaV1.5 Na+ channels in HEK cells. Whole-cell patch clamp recordings showed that zebrafish ventricular INa has better heat tolerance and slower inactivation kinetics than rainbow trout ventricular INa. In contrast, heat tolerance and inactivation kinetics of zebrafish and rainbow trout NaV1.4 channels are similar when expressed in the identical plasma membrane lipid matrix of HEK cells. The same applies to NaV1.5 channels. Thermal adaptation of the ventricular INa is largely achieved by differential expression of Na+ channel alpha subunits: zebrafish which tolerate well high temperatures mainly express the slower NaV1.5 isoform, while rainbow trout which prefer cold waters mainly express the faster NaV1.4 isoform. Differences in elasticity (stiffness) of the lipid bilayer may be also involved in thermal adaptation of INa. These findings suggest that both the protein component and its lipid bilayer matrix are involved in thermal adaptation of the voltage-gated Na+ channels and therefore in heart rate regulation under thermal stress in fish.

中文翻译:

Na +通道亚型和脂质膜环境对斑马鱼(Danio rerio)和虹鳟(Oncorhynchus mykiss)心脏Na +电流耐温性的影响

建议在鱼心脏速率的耐热性由心室的电激励受损限于由于高温对钠的拮抗效应+(I)和K +(I K1)的离子电流(I在高温压下I K1耐高温时)。为了检查Na +通道蛋白和通道的脂质基质在I Na耐热性中的作用,我们比较了斑马鱼(Danio rerio)和虹鳟(Oncorhynchus mykiss)心室I Na和I Na的温度依赖性。由克隆的斑马鱼和虹鳟鱼Na V 1.4和Na V 1.5 Na +通道在HEK细胞中产生。全细胞膜片钳记录显示,斑马鱼心室我具有较好的耐热性和失活的动力学比虹鳟鱼心室我慢。相反,当在相同的HEK细胞质膜脂质基质中表达时,斑马鱼和虹鳟鱼Na V 1.4通道的耐热性和失活动力学相似。Na V 1.5通道也是如此。心室I Na的热适应主要通过Na +的差异表达来实现通道α亚基:耐高温的斑马鱼主要表达较慢的Na V 1.5亚型,而虹鳟鱼更喜欢冷水,主要表达较快的Na V 1.4亚型。脂质双层的弹性(刚度)差异也可能涉及I Na的热适应。这些发现表明,蛋白质成分及其脂质双层基质均参与电压门控的Na +通道的热适应,因此参与鱼在热应激下的心率调节。
更新日期:2020-11-22
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