AI Article Synopsis

  • Increasing nitric oxide (NO) production dampens visual responses in retinal ganglion cells, as previously demonstrated.
  • Experiments with nNOS gene knockout mice reveal that these animals have reduced sensitivity to light, requiring higher light intensities for optimal responses compared to normal mice.
  • Overall, the findings indicate that NO levels in the retina play a critical role in modulating visual information sent to the brain, with higher NO reducing sensitivity and lack of nNOS diminishing response to light.

Article Abstract

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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http://dx.doi.org/10.1167/7.14.7DOI Listing

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