Preservation of Visual Cortex Plasticity in Retinitis Pigmentosa

T. Begenisic, R. Mazziotti, G. Sagona, L. Lupori, A. Sale, L. Galli, L. Baroncelli

Research output: Contribution to journalArticlepeer-review


Retinitis Pigmentosa (RP) is a class of inherited disorders caused by the progressive death of photoreceptors in the retina. RP is still orphan of an effective treatment, with increasing optimism deriving from research aimed at arresting neurodegeneration or replacing light-responsive elements. All these therapeutic strategies rely on the functional integrity of the visual system downstream of photoreceptors. Whereas the inner retinal structure and optic radiation are known to be considerably preserved at least in early stages of RP, very little is known about the visual cortex. Remarkably, it remains completely unclear whether visual cortex plasticity is still present in RP. Using a well-established murine model of RP, the rd10 mouse, we report that visual cortical circuits retain high levels of plasticity, preserving their capability of input-dependent remodelling even at a late stage of retinal degeneration. © 2019 IBRO
Original languageEnglish
Pages (from-to)205-210
Number of pages6
Publication statusPublished - 2020


  • plasticity
  • rd10 mouse model
  • Retinitis Pigmentosa
  • visual cortex
  • adult
  • animal cell
  • animal experiment
  • animal model
  • animal tissue
  • Article
  • brain function
  • controlled study
  • electroretinography
  • female
  • functional connectivity
  • in vitro study
  • male
  • mouse
  • nerve cell plasticity
  • nervous system electrophysiology
  • nonhuman
  • priority journal
  • retina degeneration
  • retinitis pigmentosa
  • sensory stimulation
  • synaptic transmission
  • animal
  • C57BL mouse
  • genetics
  • pathophysiology
  • physiology
  • procedures
  • retina
  • transgenic mouse
  • Animals
  • Electroretinography
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neuronal Plasticity
  • Retina
  • Visual Cortex


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