The role of activating residual neurons in recovery of vision after partial optic nerve damage

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Traumatic brain injury is a leading cause of functional loss in the central nervous system, but many deficits can be partially regained within weeks post-injury. Remarkably, only 10-20% of retinal ganglion cells (RGCs) can facilitate this recovery. Understanding how to activate residual neurons for vision recovery after partial optic nerve damage is crucial. This study utilized a defined optic nerve crush (ONC) in adult rats to explore functional recovery through behavioral and cellular methods. In vivo confocal neuroimaging (ICON) allowed for non-invasive visualization of individual RGCs, while an automated system assessed rat vision psychophysics (VIST). Key findings include: the use of dual fluorescent markers to observe retrograde axonal transport in living RGCs, revealing a temporal recovery pattern; damaged RGC axons showed intrinsic repair, with transport recovery occurring within 2-3 weeks, restoring visual function; in vivo imaging of calcium dynamics indicated that surviving RGCs exhibited a delayed, moderate calcium activation, distinct from the immediate influx seen in cell death; and visual stimulation post-ONC significantly enhanced recovery, with "visual enrichment" accelerating this process compared to normal or dark conditions. These insights underscore the importance of activating residual neurons for vision recovery, paving the way for potential therapeutic approaches.