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Wen Shen; Na-K-2Cl cotransporter deficiency in the retinas affects the visual contrast sensitivity. Invest. Ophthalmol. Vis. Sci. 2016;57(12):595.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the function of the Cl uptake co-transporter in retinal signal transduction and adaptation. To test a hypothesis that degradation of the co-transporter in the aging retina may affect the retinal electrophysiology.
The wild-type (WT) and NKCC1-deficient (NKCC1-/-) mice at age 1-4M and the WT mice at age 18-20M were used in the study. To assess the changes in retinal function, corneal flash electroretinogram (ERG) from the NKCC1-/- and WT were compared in dark- and light-adapted conditions. The influence of NKCC1 on cell membrane potential and light response were studied from horizontal cells (HCs) in intact retina. The ultimate effect of NKCC1 on the retinal signal outputs was studied in the ganglion cells (GCs) in whole-cell recording. The cell morphology, synaptic proteins and NKCC1 localization were detect in immunocytochemistry. The NKCC1 protien levels in the young and old age mouse retina were quantitatively analyzed in Western blotting.
NKCC1 was found highly expressed in the distal retina, HCs and the ON-bipolar cell dendrites, in young adult animals; but the expressing levels declined in the retinas from the old age animals. Flash ERG recordings showed that the lack of functional NKCC1 led to a reduction of the b-wave amplitude in both scotopic and photopic conditions, but oscillatory potential (OP) amplitude was unchanged, detected from the NKCC1-/- mice compared to the WT littermates. A reducing of b-wave amplitude was also observed in the old age WT animals. The cell densities and ultra-structures of photoreceptor terminals and On-bipolar cell dendrites in the NKCC1-/- retina appeared normal. However, the axon processes of HCs are reduced in the NKCC1-/- retina, although the density of HCs seems unaffected in the NKCC1-/-. The light intensity-response curve of HCs was left-shifting in the NKCC1-/-. A full range of contrast responses was tested from HCs and the GCs, showing that NKCC1 deficiency caused light-responses to saturate at relative low contrast compared to the control.
The lack of functional NKCC1 in distal retinal alters the cell communications in the retinas. Both the NKCC1-/- and old age mouse showing poor or less sensitive to contrast stimulation suggest that a deficient expression of the Cl transporter in the aging process could be one of the risk factors for age-related degradation of contrast sensitivity in vision.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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