Document Detail


Nitric oxide amplifies the rat electroretinogram.
MedLine Citation:
PMID:  20732319     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It is well established that nitric oxide (NO) participates in retinal signal processing through stimulation of its receptor enzyme, soluble guanylyl cyclase (sGC). However, under pathological conditions such as uveoretinitis, diabetic or ischemic retinopathy, elevated NO concentrations may cause protein S-nitrosation and peroxynitrite formation in the retina, promoting cellular injury and apoptosis. Previous electroretinogram (ERG) studies demonstrated deleterious effects of NO on the retinal light response, but showed no evidence for a role in normal signal processing. To better understand the function of NO in ocular physiology, we investigated the effects of exogenous NO, produced by NO donors with different release kinetics, on the flash ERG of the rat. Within a limited concentration range, NO strongly amplified ERG a- and b-waves, oscillatory potentials, and the scotopic threshold response. Amplification exceeded 100% under dark adaptation, whereas the photopic ERG and the isolated cone response were increased by less than 50%. Blocking photoreceptor-bipolar cell synapses by AP-4 demonstrated a significant increase of the isolated a-wave by NO, and modeling the ERG generator PIII supported photoreceptors as primary NO targets. The sGC inhibitors ODQ and NS2028 did not reduce NO-dependent ERG amplification, ruling out an involvement of the classical NO effector cyclic GMP. Using immunohistochemistry, we show that illumination and exogenous NO altered the S-nitrosation level of the photoreceptor layer, suggesting that direct protein modifications caused by elevated levels of NO may be responsible for the observed phenomenon.
Authors:
Alex Vielma; Luz Delgado; Claudio Elgueta; Rodrigo Osorio; Adrián G Palacios; Oliver Schmachtenberg
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-21
Journal Detail:
Title:  Experimental eye research     Volume:  91     ISSN:  1096-0007     ISO Abbreviation:  Exp. Eye Res.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-22     Completed Date:  2010-11-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370707     Medline TA:  Exp Eye Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  700-9     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso, Chile.
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MeSH Terms
Descriptor/Qualifier:
Aminobutyric Acids / pharmacology
Animals
Dark Adaptation / physiology
Electroretinography / drug effects*
Enzyme Inhibitors / pharmacology
Female
Guanylate Cyclase / antagonists & inhibitors,  metabolism
Male
Nitric Oxide / pharmacology*
Nitric Oxide Donors / pharmacology*
Nitrosation
Photic Stimulation
Photoreceptor Cells, Vertebrate / physiology
Rats
Rats, Sprague-Dawley
Retinal Bipolar Cells / physiology
Chemical
Reg. No./Substance:
0/Aminobutyric Acids; 0/Enzyme Inhibitors; 0/Nitric Oxide Donors; 10102-43-9/Nitric Oxide; 6323-99-5/2-amino-4-phosphonobutyric acid; EC 4.6.1.2/Guanylate Cyclase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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