Nitric oxide as a regulatory molecule in the processing of the visual stimulus

•NO modulating the information along the visual pathways.•cGMP-dependent nitric oxide activity amplifies the signal in retinal tissue.•In the dLGN, neuronal activity is amplified in a cGMP-independent mechanism.•On the visual cortex (V1), NO increases signal detection cGMP-dependent mechanism. Nitri...

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Bibliographic Details
Published in:Nitric oxide 2014-01, Vol.36, p.44-50
Main Authors: Lima, Monica Gomes, Maximino, Caio, Matos Oliveira, Karen Renata, Brasil, Alódia, Crespo-Lopez, Maria Elena, Batista, Evander de Jesus Oliveira, Rocha, Fernando Allan de Farias, Picanço-Diniz, Domingos Luiz Wanderley, Herculano, Anderson Manoel
Format: Article
Language:English
Subjects:
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - metabolism
Animals
Cyclic GMP - metabolism
Gene Expression Regulation
Geniculate Bodies - metabolism
Glutamine - metabolism
Humans
Lateral geniculate nucleus
N-Methylaspartate - metabolism
Neurons - metabolism
Nitric oxide
Nitric Oxide - metabolism
Primary visual cortex
Retina
Retina - metabolism
Retina - physiology
Retinal Ganglion Cells - metabolism
Signal Transduction
Vision, Ocular - physiology
Visual Cortex - metabolism
Visual processing
Visual system
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Summary:•NO modulating the information along the visual pathways.•cGMP-dependent nitric oxide activity amplifies the signal in retinal tissue.•In the dLGN, neuronal activity is amplified in a cGMP-independent mechanism.•On the visual cortex (V1), NO increases signal detection cGMP-dependent mechanism. Nitric oxide (NO) is a highly reactive gas with considerable diffusion power that is produced pre- and post synaptically in the central nervous system (CNS). In the visual system, it is involved in the processing of the visual information from the retina to superior visual centers. In this review we discuss the main mechanisms through which nitric oxide acts, in physiological levels, on the retina, lateral geniculate nucleus (LGN) and primary visual cortex. In the retina, the cGMP-dependent nitric oxide activity initially amplifies the signal, subsequently increasing the inhibitory activity, suggesting that the signal is “filtered”. In the thalamus, on dLGN, neuronal activity is amplified by NO derived from brainstem cholinergic cells, in a cGMP-independent mechanism; the result is the amplification of the signal arriving from retina. Finally, on the visual cortex (V1), NO acts through changes on the cGMP levels, increasing signal detection. These observations suggest that NO works like a filter, modulating the signal along the visual pathways.
ISSN:1089-8603
1089-8611
DOI:10.1016/j.niox.2013.10.011