May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Nitric Oxide Modulates Inhibitory Synaptic Input to Ganglion Cells in Light Adapted, Not Dark Adapted Retina
Author Affiliations & Notes
  • P.B. Cook
    Dept of Biology, Boston University, Boston, MA
  • Footnotes
    Commercial Relationships  P.B. Cook, None.
  • Footnotes
    Support  EY13400; Harcourt Charitable Foundation of MA, Boston University
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2279. doi:
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      P.B. Cook; Nitric Oxide Modulates Inhibitory Synaptic Input to Ganglion Cells in Light Adapted, Not Dark Adapted Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2279.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Background: Levels of nitric oxide (NO) in the retina are low in the dark adapted retina, are increased by steady illumination, and increased further by flashing light, but it is not known if changing levels of NO or blocking its production differ in light adapted and dark adapted retina.Purpose: I wanted to determine if synaptic inputs in the inner retina could be altered either by exogenously applied NO or by blocking NO production, and whether these effects depended on the retina’s state of adaptation. Methods: I prepared retinal slices (250–500 µm thick) using infrared imaging equipment and recorded whole–cell currents from GCs using standard patch clamp techniques. Synaptic currents were evoked with full field illumination projected through the condenser, or a focal electrical stimulus (zap) located in the outer retina. Drugs were applied through a perfusion system directed at the slice. NO synthase was blocked with LNAME (100 uM) and NO was supplied by NO donor deta–NONOate (dNO 10–100uM).Results: In dark adapted retina, application of LNAME had little or no effect on inputs to GCs, but washout frequently increased IPSCs evoked at light–OFF, and sometimes increased zap–evoked IPSCs. In light adapted retina, LNAME reduced the amplitude, increased the delay to onset, and increased the time to peak of responses at light ON. Subsequent addition of dNO reversed the effects of LNAME: it increased light–evoked inputs, decreased the delay to response onset, and decreased the time to peak, especially for IPSCs at light ON. At higher concentrations, dNO increased the duration of zap–evoked EPSCs and IPSCs, and increased the frequency of spontaneous and stimulus–evoked large IPSC spikes. Prolonged exposure (>10 min) increased the decay time of the IPSC spikes and washout of dNO rapidly eliminated IPSC spikes but zap–evoked IPSCs remained prolonged.Conclusions: In dark adapted retina NO production is low, which has been shown in imaging studies. However, NO must play some regulatory role in the dark since removing the blocker caused the retina to increase its responsiveness. In the light adapted retina NO increases the sensitivity of light responses, particularly for the ON pathway. As NO production increases, as with flashing illumination, inhibitory pathways will increase the amplitude and duration of their responses causing stronger and longer suppression of postsynaptic cells.

Keywords: ganglion cells • nitric oxide • inhibitory neurotransmitters 

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