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The Na(+)/Ca(2+), K(+) exchanger 2 modulates mammalian cone phototransduction.

Sci Rep. 2016 Sep 01;6:32521
Keisuke Sakurai 1 , Frans Vinberg 1 , Tian Wang 2 , Jeannie Chen 2 , Vladimir J Kefalov 1
Keisuke Sakurai 1 , Frans Vinberg 1 , Tian Wang 2 , Jeannie Chen 2 , Vladimir J Kefalov 1

[No authors listed]

Author information
  • 1 Department of Ophthalmology and Visual Sciences, Washington University, Saint Louis, MO 63110, USA.
  • 2 Zilkha Neurogenetic Institute, Department of Cell and Neurobiology &Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.

摘要


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.