Lack of cross modal plasticity potentially linked to ongoing activation of visual cortex and superior colliculus in the rd10 mouse model of retinitis pigmentosa.

Efforts in vision restoration have been focused on a condition called Retinitis Pigmentosa, where photoreceptors in the retina degenerate while the rest of the visual pathway remain mostly intact. Retinal implants that directly stimulate retinal ganglion cells have shown promising but limited results in patients so far. Apart from technical limitations, cross-modal plasticity of visual areas might contribute to this problem. We therefore investigated if the primary visual cortex (V1) of the rd10 mouse model for retinal degeneration became more sensitive to auditory or tactile sensory inputs. After reaching complete blindness confirmed by the lack of optomotor responses, activity in V1 and superior colliculus (SC) was recorded using Neuropixels probes. While we could not find any significant differences in tactile or auditory responses compared to wildtype mice, the local field potential revealed distinct oscillatory events (0.5-6 Hz) in V1 and SC resembling previously observed aberrant activity in the retina of rd10 mice. We therefore propose that aberrant retinal activity is transmitted to higher visual areas where it prevents cross-modal changes. Additionally, our results provide evidence of an intact visual cortex with promising potential for future therapeutic strategies to restore vision.