Emergence of Sustained Spontaneous Hyperactivity and Temporary Preservation of off Responses in Ganglion Cells of the Retinal Degeneration (rd1) Mouse

TL;DR: Oscillatory activity in healthy retinas shares many features with the functional phenotype detected in rd10 retinas, and quantitative physiological differences advance the understanding of the degeneration process and may guide future rescue strategies.

TL;DR: The response differences between cell types suggest some forms of preferential activation may be possible, and further testing is warranted, and the scope of the response differences found here suggests activation mechanisms that are more complex than those described in previous studies.

TL;DR: The extent of functional remodeling in the retina following rod death but before cone loss is identified, and new potential challenges to restoring normal vision by replacing lost rod photoreceptors are indicated.

TL;DR: Compared spontaneous and light-evoked activity among retinal ganglion cells in rd1 and rd10 mice, strains with closely related retinal disease, raises hope that visual function might be preserved or restored despiteganglion cell hyperactivity seen in inherited retinal degenerations, particularly if treatment or manipulation of early developmental plasticity were to be timed appropriately.

TL;DR: Retinal remodeling is not plasticity, but represents the invocation of mechanisms resembling developmental and CNS plasticities and together, neuronal remodeling and the formation of the glial seal may abrogate many cellular and bionic rescue strategies.

TL;DR: The cpfl1 mutation is the first naturally-arising mutation in mice to cause cone-specific photoreceptor function loss and may provide a model for congenital achromatopsia in humans.

TL;DR: Cortical prostheses will be described only because of their direct effect on the concept and technical development of the other prostheses, and this will be done in a more general and historic perspective.

TL;DR: Data presented represent direct proof that electrical synapses are critical for the propagation of rod signals across the mammalian retina, and they demonstrate the existence of multiple rod pathways, each of which is dependent on electricalsynapses.