The sensitivity of light-evoked responses of retinal ganglion cells is decreased in nitric oxide synthase gene knockout mice

We have shown previously that increasing the production of nitric oxide (NO) results in a dampening of visual responses of retinal ganglion cells (G. Y. Wang, L. C. Liets, & L. M. Chalupa, 2003). To gain further insights into the role of NO in retinal function, we made whole-cell patch clamp rec...

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Veröffentlicht in:Journal of vision (Charlottesville, Va.) Va.), 2007-11, Vol.7 (14), p.7.1
Hauptverfasser: Wang, Guo-Yong, van der List, Deborah A, Nemargut, Joseph P, Coombs, Julie L, Chalupa, Leo M
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container_issue 14
container_start_page 7.1
container_title Journal of vision (Charlottesville, Va.)
container_volume 7
creator Wang, Guo-Yong
van der List, Deborah A
Nemargut, Joseph P
Coombs, Julie L
Chalupa, Leo M
description We have shown previously that increasing the production of nitric oxide (NO) results in a dampening of visual responses of retinal ganglion cells (G. Y. Wang, L. C. Liets, & L. M. Chalupa, 2003). To gain further insights into the role of NO in retinal function, we made whole-cell patch clamp recordings from ganglion cells of neural type nitric oxide synthase (nNOS) gene knockout mice. Here we show that in the dark-adapted state, the sensitivity of retinal ganglion cell to light stimulation is decreased in nNOS knockout animals. The lowest light intensities required to evoke optimal responses and the average intensities that evoked half-maximal responses were significantly higher in nNOS knockouts than in normal mice. Retinal histology and other features of light-evoked responses of ganglion cells in nNOS mice appeared to be indistinguishable from those of normal mice. Collectively, these results, in conjunction with our previous work, provide evidence that increasing levels of NO dampen visual responses of ganglion cells, while a lack of nNOS decreases the sensitivity of these neurons to light. Thus, NO levels in the retina are capable of modulating the information that ganglion cells convey to the visual centers of the brain.
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Y. Wang, L. C. Liets, &amp; L. M. Chalupa, 2003). To gain further insights into the role of NO in retinal function, we made whole-cell patch clamp recordings from ganglion cells of neural type nitric oxide synthase (nNOS) gene knockout mice. Here we show that in the dark-adapted state, the sensitivity of retinal ganglion cell to light stimulation is decreased in nNOS knockout animals. The lowest light intensities required to evoke optimal responses and the average intensities that evoked half-maximal responses were significantly higher in nNOS knockouts than in normal mice. Retinal histology and other features of light-evoked responses of ganglion cells in nNOS mice appeared to be indistinguishable from those of normal mice. Collectively, these results, in conjunction with our previous work, provide evidence that increasing levels of NO dampen visual responses of ganglion cells, while a lack of nNOS decreases the sensitivity of these neurons to light. 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subjects Action Potentials - drug effects
Amacrine Cells - cytology
Amacrine Cells - enzymology
Animals
Arginine - pharmacology
Dark Adaptation - physiology
Dose-Response Relationship, Radiation
Enzyme Inhibitors - pharmacology
Immunologic Techniques
In Vitro Techniques
Light
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Neurological
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide Synthase Type I - deficiency
Nitric Oxide Synthase Type I - metabolism
Patch-Clamp Techniques
Retina - cytology
Retina - metabolism
Retinal Ganglion Cells - drug effects
Retinal Ganglion Cells - physiology
Retinal Ganglion Cells - radiation effects
Signal Transduction - physiology
Staining and Labeling
title The sensitivity of light-evoked responses of retinal ganglion cells is decreased in nitric oxide synthase gene knockout mice
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