NO signaling in retinal bipolar cells. (August 2017)

• Record Type: Journal Article
• Authors: Agurto, A.; Vielma, A.H.; Cadiz, B.; Couve, E.; Schmachtenberg, O.
• Is Part Of: Experimental eye research. Volume 161(2017)
• Page Start: 30
• Page End: 35
• Publication Date: 2017-08
• Subjects: NO -- Retina -- Vision -- Bipolar cell -- DAF-FM -- Soluble guanylate cyclase; BC bipolar cell -- RBC rod bipolar cell -- NO nitric oxide -- NOS NO synthase -- DAF 4-Amino-5-methylamino-2′, 7′-difluorofluorescein -- IPL inner plexiform layer -- INL inner nuclear layer -- GCL ganglion cell layer -- sGC soluble guanylate cyclase; Ophthalmology -- Periodicals; Eye -- Periodicals; Œil -- Périodiques; Ophthalmology; Periodicals; Electronic journals; 612.8405
• DOI: 10.1016/j.exer.2017.05.013
• Languages: English
• ISSNs: 0014-4835

Abstract

Abstract: Nitric oxide (NO) is a neuromodulator involved in physiological and pathological processes in the retina. In the inner retina, a subgroup of amacrine cells have been shown to synthesize NO, but bipolar cells remain controversial as NO sources. This study correlates NO synthesis in dark-adapted retinas, through labeling with the NO marker DAF-FM, with neuronal nitric oxide synthase (nNOS) and inducible NOS expression, and presence of the NO receptor soluble guanylate cyclase in bipolar cells. NO containing bipolar cells were morphologically identified by dialysis of DAF fluorescent cells with intracellular dyes, or by DAF labeling followed by immunohistochemistry for nNOS and other cellular markers. DAF fluorescence was observed in all types of bipolar cells that could be identified, but the most intense DAF fluorescence was observed in bipolar cells with severed processes, supporting pathological NO signaling. Among nNOS expressing bipolar cells, type 9 was confirmed unequivocally, while types 2, 3a, 3b, 4, 5, 7, 8 and the rod bipolar cell were devoid of this enzyme. These results establish specific bipolar cell types as NO sources in the inner retina, and support the involvement of NO signaling in physiological and pathological processes in the inner retina.