Medical School, Newcastle University Biosciences Institute, Newcastle upon Tyne, UK.
Department of Cell Biology and Physiology, Brigham Young University, Provo, Utah, USA.
Physiol Rep. 2023 Aug;11(15):e15778. doi: 10.14814/phy2.15778.
We recently reported that strong activation of the optogenetic chloride pump, halorhodopsin leads to a secondary redistribution of K ions into the cell, through tonically open, "leak" K channels. Here we show that this effect is not unique to halorhodopsin but is also seen with activation of another electrogenic ion pump, archaerhodopsin. The two opsins differ however in the size of the rebound rise in extracellular potassium, [K ] , after the end of activation, which is far larger with halorhodopsin than for archaerhodopsin activation. Multiple linear regression modeling indicates that the variance in the postillumination surge in [K ] was explained both by the size of the preceding, illumination-induced drop in [K ] and also by the type of opsin. These data provide additional support for the hypothesis that intense chloride-loading of cells, as occurs naturally following intense bursts of GABAergic synaptic bombardment, or artificially following halorhodopsin activation, is followed by extrusion of both Cl and K coupled together. We discuss this with respect to the pattern of [K ] rise that occurs at the onset of seizure-like events.
我们最近报道称,光遗传学氯离子泵 halorhodopsin 的强烈激活会导致钾离子通过持续开放的“泄漏”钾通道重新分布到细胞内。在这里,我们表明这种效应并非 halorhodopsin 所特有,也可以在另一种电致离子泵 archaeerhodopsin 的激活中观察到。然而,这两种光感受器在激活结束后细胞外钾离子 [K+] 的反弹上升幅度上存在差异,halorhodopsin 的上升幅度远大于 archaeerhodopsin。多元线性回归模型表明,光照诱导的 [K+] 下降幅度和光感受器类型都可以解释 [K+] 在后照光期间上升的方差。这些数据为以下假设提供了额外的支持,即在 GABA 能突触强烈冲击后或人工激活 halorhodopsin 后细胞内氯离子的强烈加载,随后氯离子和钾离子共同被排出。我们将其与癫痫样事件开始时发生的 [K+] 上升模式进行了讨论。