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光照后视杆光感受器中的适应性增强。

Adaptive potentiation in rod photoreceptors after light exposure.

作者信息

McKeown Alex S, Kraft Timothy W

机构信息

Department of Vision Sciences, University of Alabama at Birmingham, Birmingham, AL 35294.

Department of Vision Sciences, University of Alabama at Birmingham, Birmingham, AL 35294

出版信息

J Gen Physiol. 2014 Jun;143(6):733-43. doi: 10.1085/jgp.201411163. Epub 2014 May 12.

Abstract

Photoreceptors adapt to changes in illumination by altering transduction kinetics and sensitivity, thereby extending their working range. We describe a previously unknown form of rod photoreceptor adaptation in wild-type (WT) mice that manifests as a potentiation of the light response after periods of conditioning light exposure. We characterize the stimulus conditions that evoke this graded hypersensitivity and examine the molecular mechanisms of adaptation underlying the phenomenon. After exposure to periods of saturating illumination, rods show a 10-35% increase in circulating dark current, an adaptive potentiation (AP) to light exposure. This potentiation grows as exposure to light is extended up to 3 min and decreases with longer exposures. Cells return to their initial dark-adapted sensitivity with a time constant of recovery of ∼7 s. Halving the extracellular Mg concentration prolongs the adaptation, increasing the time constant of recovery to 13.3 s, but does not affect the magnitude of potentiation. In rods lacking guanylate cyclase activating proteins 1 and 2 (GCAP(-/-)), AP is more than doubled compared with WT rods, and halving the extracellular Mg concentration does not affect the recovery time constant. Rods from a mouse expressing cyclic nucleotide-gated channels incapable of binding calmodulin also showed a marked increase in the amplitude of AP. Application of an insulin-like growth factor-1 receptor (IGF-1R) kinase inhibitor (Tyrphostin AG1024) blocked AP, whereas application of an insulin receptor kinase inhibitor (HNMPA(AM)3) failed to do so. A broad-acting tyrosine phosphatase inhibitor (orthovanadate) also blocked AP. Our findings identify a unique form of adaptation in photoreceptors, so that they show transient hypersensitivity to light, and are consistent with a model in which light history, acting via the IGF-1R, can increase the sensitivity of rod photoreceptors, whereas the photocurrent overshoot is regulated by Ca-calmodulin and Ca(2+)/Mg(2+)-sensitive GCAPs.

摘要

光感受器通过改变转导动力学和敏感性来适应光照变化,从而扩展其工作范围。我们在野生型(WT)小鼠中描述了一种以前未知的视杆光感受器适应形式,其表现为在经过一定时间的适应性光照暴露后光反应的增强。我们对引发这种分级超敏反应的刺激条件进行了表征,并研究了该现象背后的适应分子机制。在暴露于饱和光照一段时间后,视杆细胞的循环暗电流增加10%-35%,这是对光照的一种适应性增强(AP)。这种增强随着光照暴露时间延长至3分钟而增加,并随着更长时间的暴露而降低。细胞以约7秒的恢复时间常数恢复到其初始暗适应敏感性。将细胞外镁浓度减半会延长适应时间,使恢复时间常数增加到13.3秒,但不影响增强幅度。在缺乏鸟苷酸环化酶激活蛋白1和2(GCAP(-/-))的视杆细胞中,与野生型视杆细胞相比,AP增加了一倍多,并且将细胞外镁浓度减半不影响恢复时间常数。来自表达不能结合钙调蛋白的环核苷酸门控通道的小鼠的视杆细胞也显示出AP幅度的显著增加。应用胰岛素样生长因子-1受体(IGF-1R)激酶抑制剂(酪氨酸磷酸化抑制剂AG1024)可阻断AP,而应用胰岛素受体激酶抑制剂(HNMPA(AM)3)则不能。一种广泛作用的酪氨酸磷酸酶抑制剂(原钒酸盐)也可阻断AP。我们的研究结果确定了光感受器中一种独特的适应形式,即它们对光表现出短暂的超敏反应,并且与一种模型一致,在该模型中,光照历史通过IGF-1R起作用,可以增加视杆光感受器的敏感性,而光电流过冲则由钙-钙调蛋白和Ca(2+)/Mg(2+)-敏感的GCAPs调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36fe/4035749/9a7822e62a37/JGP_201411163_Fig3.jpg

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