ArticleScientific reports2016
The Na(+)/Ca(2+), K(+) exchanger 2 modulates mammalian cone phototransduction.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
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- The Logistical Backbone of Photoreceptor Cell Function: Complementary Mechanisms of Dietary Vitamin A Receptors and Rhodopsin Transporters.International journal of molecular sciences · 2024Review
- Light drives the developmental progression of outer retinal function.The Journal of general physiology · 2023Article
- Visual pigment-deficient cones survive and mediate visual signaling despite the lack of outer segments.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Biochemistry and physiology of zebrafish photoreceptors.Pflugers Archiv : European journal of physiology · 2021Review
- Ex vivo electroretinograms made easy: performing ERGs using 3D printed components.The Journal of physiology · 2020Article
- Regulation of calcium homeostasis in the outer segments of rod and cone photoreceptors.Progress in retinal and eye research · 2018Review
- Guanylate cyclase-activating protein 2 contributes to phototransduction and light adaptation in mouse cone photoreceptors.The Journal of biological chemistry · 2018Article
- Expression of potassium-dependent sodium-calcium exchanger in the murine lens.Experimental eye research · 2018Article
- The NaeLife · 2017Article
- Mitochondria Maintain Distinct CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Calcium ions (Ca(2+)) modulate the phototransduction cascade of vertebrate cone photoreceptors to tune gain, inactivation, and light adaptation. In darkness, the continuous current entering the cone outer segment through cGMP-gated (CNG) channels is carried in part by Ca(2+), which is then extruded back to the extracellular space. The mechanism of Ca(2+) extrusion from mammalian cones is not understood. The dominant view has been that the cone-specific isoform of the Na(+)/Ca(2+), K(+) exchanger, NCKX2, is responsible for removing Ca(2+) from their outer segments. However, indirect evaluation of cone function in NCKX2-deficient (Nckx2(-/-)) mice by electroretinogram recordings revealed normal photopic b-wave responses. This unexpected result suggested that NCKX2 may not be involved in the Ca(2+) homeostasis of mammalian cones. To address this controversy, we examined the expression of NCKX2 in mouse cones and performed transretinal recordings from Nckx2(-/-) mice to determine the effect of NCKX2 deletion on cone function directly. We found that Nckx2(-/-) cones exhibit compromised phototransduction inactivation, slower response recovery and delayed background adaptation. We conclude that NCKX2 is required for the maintenance of efficient Ca(2+) extrusion from mouse cones. However, surprisingly, Nckx2(-/-) cones adapted normally in steady background light, indicating the existence of additional Ca(2+)-extruding mechanisms in mammalian cones.
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