Nitric oxide amplifies the rat electroretinogram

Vielma, A; Delgado L.; Elgueta, C; Osorio, R; Palacios, AG; Schmachtenberg, O.

Abstract

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. © 2010 Elsevier Ltd.

Más información

Título según WOS: Nitric oxide amplifies the rat electroretinogram
Título según SCOPUS: Nitric oxide amplifies the rat electroretinogram
Título de la Revista: EXPERIMENTAL EYE RESEARCH
Volumen: 91
Número: 5
Editorial: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Fecha de publicación: 2010
Página de inicio: 700
Página final: 709
Idioma: English
URL: http://linkinghub.elsevier.com/retrieve/pii/S0014483510002587
DOI:

10.1016/j.exer.2010.08.014

Notas: ISI, SCOPUS