Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Adv Exp Med Biol. 2012;740:873-89. doi: 10.1007/978-94-007-2888-2_39.
This review lays out the emerging evidence for the fundamental role of Ca(2+) stores and store-operated channels in the Ca(2+) homeostasis of rods and cones. Calcium-induced calcium release (CICR) is a major contributor to steady-state and light-evoked photoreceptor Ca(2+) homeostasis in the darkness whereas store-operated Ca(2+) channels play a more significant role under sustained illumination conditions. The homeostatic response includes dynamic interactions between the plasma membrane, endoplasmic reticulum (ER), mitochondria and/or outer segment disk organelles which dynamically sequester, accumulate and release Ca(2+). Coordinated activation of SERCA transporters, ryanodine receptors (RyR), inositol triphosphate receptors (IP3Rs) and TRPC channels amplifies cytosolic voltage-operated signals but also provides a memory trace of previous exposures to light. Store-operated channels, activated by the STIM1 sensor, prevent pathological decrease in [Ca(2+)]i mediated by excessive activation of PMCA transporters in saturating light. CICR and SOCE may also modulate the transmission of afferent and efferent signals in the outer retina. Thus, Ca(2+) stores provide additional complexity, adaptability, tuneability and speed to photoreceptor signaling.
这篇综述阐述了钙储存库和钙库操纵性通道在视杆和视锥细胞钙离子稳态中的基本作用的新证据。钙诱导钙释放（CICR）是暗适应中稳态和光诱发光感受器钙离子稳态的主要贡献者，而在持续光照条件下，钙库操纵性通道则发挥更重要的作用。内稳态反应包括质膜、内质网（ER）、线粒体和/或外节盘状细胞器之间的动态相互作用，这些细胞器动态地隔离、积累和释放钙离子。SERCA 转运体、ryanodine 受体（RyR）、三磷酸肌醇受体（IP3Rs）和 TRPC 通道的协调激活放大了细胞质电压门控信号，但也提供了对先前光暴露的记忆痕迹。由 STIM1 传感器激活的钙库操纵性通道可防止在饱和光下 PMCA 转运体过度激活介导的病理性 [Ca2+]i 降低。CICR 和 SOCE 也可能调节外视网膜中传入和传出信号的传递。因此，钙储存库为光感受器信号提供了额外的复杂性、适应性、可调性和速度。
