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N. Cuenca, G. C. Martínez-Navarrete, J. Esteve-Rudd, A. Angulo, I. Pinilla, J. Martín-Nieto; Connexin 36 Distribution Pattern in the Vertebrate Retina: Impaired Expression in Retinitis Pigmentosa Rodent Models. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5942.
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In the vertebrate retina communication between neurons through gap junctions is involved in light adaptation and in the transfer of visual information from the rod to the cone pathway. Connexin 36 (Cx36) is a protein forming part of gap junctions established between vertebrate neurons. We have characterized the distribution pattern of Cx36 in rod- and cone-dominant retinas and their expression in rodent models of retinitis pigmentosa.
Cryostat retinal sections from different vertebrate species, and from rodents exhibiting retinitis pigmentosa (rd1, rd10 mice; RCS, P23H, S334ter rats) were doubly immunolabeled with antibodies against Cx36, recoverin, PKC, calretinin and parvalbumin. After incubation with secondary antibodies, images were obtained by fluorescent confocal microscopy.
In all species studied Cx36 was present in both plexiform layers, although lesser immunoreactivity was found in the IPL in lower vertebrates. In species with scotopic vision, Cx36 formed part mostly of homologous gap junctions established between the dendrites of AII amacrine cells. Cx36 was also associated with axon terminals of rod bipolar cells. In the retina of the squirrel, Cx36-positive puncta were found both in the OPL and between the cell bodies of cones and rods in the ONL. In cone-dominant retinas Cx36 expression was significantly lower in the IPL, with immunoreactivity being mainly associated with cone bipolar cells. Cx36 levels were significantly diminished in the IPL of both mouse and rat models of retinitis pigmentosa.
In species with photopic vision, which bear a cone-dominant retina lacking AII cells, Cx36 distributed mainly in the outer retina, and in the IPL was predominantly associated with cone bipolars. By contrast, in mammals with scotopic vision Cx36 mostly located to AII dendrites and, interestingly, at both cone- and rod-bipolar axon terminals. A loss of Cx36 gap junctions between AII amacrines, and thus an impaired rod visual pathway, was found in retinitis pigmentosa animal models.Support: MEC BFU2006-00957/BFI, GV06/197, ONCE and FUNDALUCE.
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