Visual Cortex Engagement in Retinitis Pigmentosa |
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Authors: | Gianluca Pietra Tiziana Bonifacino Davide Talamonti Giambattista Bonanno Alessandro Sale Lucia Galli Laura Baroncelli |
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Affiliation: | 1.Neuroscience Institute, National Research Council (CNR), I-56124 Pisa, Italy; (G.P.); (D.T.); (A.S.); (L.G.);2.Section of Pharmacology and Toxicology Unit, Department of Pharmacy, University of Genova, I-16148 Genova, Italy; (T.B.); (G.B.);3.Department of Life Science, University of Trieste, I-34128 Trieste, Italy;4.IRCCS Ospedale Policlinico San Martino, I-16132 Genova, Italy;5.Department of Developmental Neuroscience, IRCCS Stella Maris Foundation, I-56128 Pisa, Italy |
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Abstract: | Retinitis pigmentosa (RP) is a family of inherited disorders caused by the progressive degeneration of retinal photoreceptors. There is no cure for RP, but recent research advances have provided promising results from many clinical trials. All these therapeutic strategies are focused on preserving existing photoreceptors or substituting light-responsive elements. Vision recovery, however, strongly relies on the anatomical and functional integrity of the visual system beyond photoreceptors. Although the retinal structure and optic pathway are substantially preserved at least in early stages of RP, studies describing the visual cortex status are missing. Using a well-established mouse model of RP, we analyzed the response of visual cortical circuits to the progressive degeneration of photoreceptors. We demonstrated that the visual cortex goes through a transient and previously undescribed alteration in the local excitation/inhibition balance, with a net shift towards increased intracortical inhibition leading to improved filtering and decoding of corrupted visual inputs. These results suggest a compensatory action of the visual cortex that increases the range of residual visual sensitivity in RP. |
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Keywords: | retinitis pigmentosa visual cortex plasticity inhibition rd10 mouse model |
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