Schmitz Frank
Department of Neuroanatomy, Institute for Anatomy and Cell Biology, Medical School Homburg/Saar, Saarland University Saarland, Germany.
Front Mol Neurosci. 2014 Feb 6;7:3. doi: 10.3389/fnmol.2014.00003. eCollection 2014.
Changes in intracellular calcium ions [Ca(2+)] play important roles in photoreceptor signaling. Consequently, intracellular [Ca(2+)] levels need to be tightly controlled. In the light-sensitive outer segments (OS) of photoreceptors, Ca(2+) regulates the activity of retinal guanylate cyclases thus playing a central role in phototransduction and light-adaptation by restoring light-induced decreases in cGMP. In the synaptic terminals, changes of intracellular Ca(2+) trigger various aspects of neurotransmission. Photoreceptors employ tonically active ribbon synapses that encode light-induced, graded changes of membrane potential into modulation of continuous synaptic vesicle exocytosis. The active zones of ribbon synapses contain large electron-dense structures, synaptic ribbons, that are associated with large numbers of synaptic vesicles. Synaptic coding at ribbon synapses differs from synaptic coding at conventional (phasic) synapses. Recent studies revealed new insights how synaptic ribbons are involved in this process. This review focuses on the regulation of [Ca(2+)] in presynaptic photoreceptor terminals and on the function of a particular Ca(2+)-regulated protein, the neuronal calcium sensor protein GCAP2 (guanylate cyclase-activating protein-2) in the photoreceptor ribbon synapse. GCAP2, an EF-hand-containing protein plays multiple roles in the OS and in the photoreceptor synapse. In the OS, GCAP2 works as a Ca(2+)-sensor within a Ca(2+)-regulated feedback loop that adjusts cGMP levels. In the photoreceptor synapse, GCAP2 binds to RIBEYE, a component of synaptic ribbons, and mediates Ca(2+)-dependent plasticity at that site. Possible mechanisms are discussed.
细胞内钙离子[Ca(2+)]的变化在光感受器信号传导中起重要作用。因此，细胞内[Ca(2+)]水平需要受到严格控制。在光感受器的光敏外段（OS）中，Ca(2+)调节视网膜鸟苷酸环化酶的活性，从而通过恢复光诱导的cGMP降低在光转导和光适应中发挥核心作用。在突触末端，细胞内Ca(2+)的变化触发神经传递的各个方面。光感受器采用持续活跃的带状突触，将光诱导的膜电位分级变化编码为连续突触小泡胞吐作用的调节。带状突触的活性区包含大的电子致密结构，即突触带，其与大量突触小泡相关。带状突触的突触编码不同于传统（相位）突触的突触编码。最近的研究揭示了关于突触带如何参与这一过程的新见解。本综述重点关注突触前光感受器末端[Ca(2+)]的调节以及特定的Ca(2+)调节蛋白——神经元钙传感器蛋白GCAP2（鸟苷酸环化酶激活蛋白-2）在光感受器带状突触中的功能。GCAP2是一种含EF手结构的蛋白在OS和光感受器突触中发挥多种作用。在OS中，GCAP2在调节cGMP水平的Ca(2+)调节反馈回路中作为Ca(2+)传感器起作用。在光感受器突触中，GCAP2与突触带的一个成分RIBEYE结合，并介导该部位的Ca(2+)依赖性可塑性。文中讨论了可能的机制。
