Identification of alternate transcripts of neuronal nitric oxide synthase in the mouse retina

Giove, Thomas J.; Deshpande, Monika; Eldred, William D.

doi:10.1002/jnr.22133

Cited by 30 publications

(40 citation statements)

References 50 publications

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“…Unlike ΔI C , the light-evoked ΔI Cl that represents the inhibitory inputs from ACs was relatively small in these NOACs. The results are also in line with the previous reports that retinal NO release (detected by DAF fluorescency), is enhanced by light, especially by flashing light (Eldred and Blute, 2005; Giove, et al, 2009). …”

Section: Discussionsupporting

confidence: 93%

“…However, there is still some conflict regarding its diffusion. By using DAF (diaminofluoresceins) NO fluorescency, some studies showed that NO generated from ACs were restricted in the cells in turtle retina (Eldred and Blute, 2005) and NO did not diffuse in the mouse retina (Giove et al, 2009). The underlying mechanism is not clear.…”

Section: Introductionmentioning

confidence: 99%

“…Retinal NO DAF fluorescence has been found to be enhanced by light in the mouse and turtle retina (Eldred and Blute, 2005; Giove, et al, 2009); but it is still unclear how NO release from a NOAC is specifically related to physiological stimuli (e.g. light) or pathological signals.…”

Section: Introductionmentioning

confidence: 99%

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Light responses and morphology of bNOS‐immunoreactive neurons in the mouse retina

Pang

2010

J of Comparative Neurology

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Nitric oxide (NO), produced by NO synthase (NOS), modulates the function of all retinal neurons and ocular blood vessels and participates in the pathogenesis of ocular diseases. To further understand the regulation of ocular NO release, we systematically studied the morphology, topography and light responses of NOS-containing amacrine cells (NOACs) in dark-adapted mouse retina. Immunohistological staining for neuronal NOS (bNOS), combined with retrograde labeling of ganglion cells (GCs) with Neurobiotin (NB, a gap junction permeable dye) and Lucifer yellow (LY, a less permeable dye), was used to identify NOACs. The light responses of ACs were recorded under whole-cell voltage clamp conditions and cell morphology was examined with a confocal microscope. We found that in dark-adapted conditions bNOS-immunoreactivity (IR) was present primarily in the inner nuclear layer and the ganglion cell layer. bNOS-IR somas were negative for LY, thus they were identified as ACs; nearly 6 % of the cells were labeled by NB but not by LY, indicating that they were dye-coupled with GCs. Three morphological subtypes of NOACs (NI, NII and displaced) were identified. The cell density, inter-cellular distance and the distribution of NOACs were studied in whole retinas. Light evoked depolarizing highly sensitive ON-OFF responses in NI cells and less sensitive OFF responses in NII cells. Frequent (1 to 2 Hz) or abrupt change of light-intensity evoked larger peak responses. The possibility for light to modify NO release from NOACs is discussed.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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Light responses and morphology of bNOS‐immunoreactive neurons in the mouse retina

Pang

2010

J of Comparative Neurology

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“…[14][15][16][17][18][19][20][21][22][23] In the excited Cco complex O 2 binding is favored over NO binding, and oxidative phosphorylation increases as a result of an increase in the rate of O 2 reduction. The interaction between NO and Cco has been shown to be light sensitive across various mitochondrial oxidative milieu, 17,20,[23][24][25][26] and NO-induced regulation of apoptosis, both positive and negative, has also been observed. 21,[27][28][29][30] Since we have observed changes in expression of apoptosis genes in retinal pigmented epithelial cells after exposing them to red light in vitro, we decided to look for changes in intracellular levels of NO and ATP.…”

Section: Introductionmentioning

confidence: 93%

The response of human retinal pigmented epithelial cells in vitro to changes in nitric oxide concentration stimulated by low levels of red light

Lavey

Estlack

Schuster³

et al. 2013

SPIE Proceedings

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The goal of this project is to explore the role of nitric oxide (NO) in regulating the response of hTERT-RPE to low-level exposures to red light. Exposure to low-level red light has been shown to positively affect wound healing, reduce pain, and encourage cell proliferation. The current explanation for this effect is described as an interaction between the photons and cytochrome c oxidase (Cco), which plays a role in regulation of intracellular NO levels in addition to being the mitochondrial protein complex where reduction of oxygen occurs in the process of oxidative phosphorylation. Exposure to 2.88 J/cm 2 of 671-nm and 637-nm light shows a two-fold increase in NO immediately after exposure, and a 56% increase in ATP measured at ~5 h post exposure. Levels of NF-κB mRNA and protein were measured at six and 24 h, respectively, and found to increase six fold, correlating with increases in NO levels. Light-stimulated increased levels of NO also correlated with an 11-fold increase in Bcl-2 and a 70% decrease in Bax mRNA levels, relative to controls. NF-κB promotes cell growth and Bcl-2 is an apoptosis suppressor protein. Bax is a positive apoptotic effector protein.These results support the hypothesis that light-induced changes in the intracellular levels of NO play a role in the beneficial effects of low-level light photobiomodulation

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“…15 However, another receptor for red and NIR light has been proposed for retinal cells: neuronal nitric oxide synthase (nNOS). [16][17][18] Two other NOS isozymes are also known to occur in mammalian cells: endothelial NOS (eNOS) and induced NOS (iNOS). 19 Nitric oxide is also produced in the mitochondria, ostensibly by a mitochondrial NOS.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide measurements in hTERT-RPE cells and subcellular fractions exposed to low levels of red light

Wigle

Castellanos²,

Denton³

et al. 2014

SPIE Proceedings

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Cells in a tissue culture model for laser eye injury exhibit increased resistance to a lethal pulse of 2.0-μm laser radiation if the cells are first exposed to 2.88 J/cm 2 of red light 24 hr prior to the lethal laser exposure. Changes in expression of various genes associated with apoptosis have been observed, but the biochemical link between light absorption and gene expression remains unknown. Cytochome c oxidase (CCOX), in the electron transport chain, is the currentlyhypothesized absorber. Absorption of the red light by CCOX is thought to facilitate displacement of nitric oxide (NO) by O 2 in the active site, increasing cellular respiration and intracellular ATP. However, NO is also an important regulator and mediator of numerous physiological processes in a variety of cell and tissue types that is synthesized from l-arginine by NO synthases. In an effort to determine the relative NO contributions from these competing pathways, we measured NO levels in whole cells and subcellular fractions, with and without exposure to red light, using DAF-FM, a fluorescent dye that stoichiometrically reacts with NO. Red light induced a small, but consistently reproducible, increase in fluorescence intensity in whole cells and some subcellular fractions. Whole cells exhibited the highest overall fluorescence intensity followed by (in order) cytosolic proteins, microsomes, then nuclei and mitochondria.

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Identification of alternate transcripts of neuronal nitric oxide synthase in the mouse retina

Cited by 30 publications

References 50 publications

Light responses and morphology of bNOS‐immunoreactive neurons in the mouse retina

Light responses and morphology of bNOS‐immunoreactive neurons in the mouse retina

The response of human retinal pigmented epithelial cells in vitro to changes in nitric oxide concentration stimulated by low levels of red light

Nitric oxide measurements in hTERT-RPE cells and subcellular fractions exposed to low levels of red light

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