Nogo-A deletion increases the plasticity of the optokinetic response and changes retinal projection organization in the adult mouse visual system

Brain Struct Funct. 2016 Jan;221(1):317-29. doi: 10.1007/s00429-014-0909-3. Epub 2014 Oct 5.


The inhibitory action of Nogo-A on axonal growth has been well described. However, much less is known about the effects that Nogo-A could exert on the plasticity of neuronal circuits under physiological conditions. We investigated the effects of Nogo-A knock-out (KO) on visual function of adult mice using the optokinetic response (OKR) and the monocular deprivation (MD)-induced OKR plasticity and analyzed the anatomical organization of the eye-specific retinal projections. The spatial frequency sensitivity was higher in intact Nogo-A KO than in wild-type (WT) mice. After MD, Nogo-A KO mice reached a significantly higher spatial frequency and contrast sensitivity. Bilateral ablation of the visual cortex did not affect the OKR sensitivity before MD but reduced the MD-induced enhancement of OKR by approximately 50% in Nogo-A KO and WT mice. These results suggest that cortical and subcortical brain structures contribute to the OKR plasticity. The tracing of retinal projections to the dorsal lateral geniculate nucleus (dLGN) revealed that the segregation of eye-specific terminals was decreased in the adult Nogo-A KO dLGN compared with WT mice. Strikingly, MD of the right eye led to additional desegregation of retinal projections in the left dLGN of Nogo-A KO but not in WT mice. In particular, MD promoted ectopic varicosity formation in Nogo-A KO dLGN axons. The present data show that Nogo-A restricts visual experience-driven plasticity of the OKR and plays a role in the segregation and maintenance of retinal projections to the brain.

Keywords: Monocular deprivation; Optokinetic response; Plasticity; Retinogeniculate projections; Subcortical visual system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blindness / genetics
  • Blindness / metabolism*
  • Blindness / physiopathology
  • Contrast Sensitivity
  • Disease Models, Animal
  • Gene Deletion
  • Genotype
  • Male
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myelin Proteins / deficiency*
  • Myelin Proteins / genetics
  • Neuronal Plasticity*
  • Nogo Proteins
  • Nystagmus, Optokinetic*
  • Optic Nerve / metabolism*
  • Optic Nerve / physiopathology
  • Phenotype
  • Photic Stimulation
  • Retina / metabolism*
  • Retina / physiopathology
  • Spatial Navigation
  • Time Factors
  • Vision, Ocular*
  • Visual Cortex / metabolism*
  • Visual Cortex / physiopathology
  • Visual Cortex / surgery
  • Visual Pathways / metabolism
  • Visual Pathways / physiopathology


  • Myelin Proteins
  • Nogo Proteins
  • Rtn4 protein, mouse