Current Biology
Volume 28, Issue 12, 18 June 2018, Pages 1914-1923.e5
Journal home page for Current Biology

Article
Distinct Circuits for Recovery of Eye Dominance and Acuity in Murine Amblyopia

https://doi.org/10.1016/j.cub.2018.04.055Get rights and content
Under an Elsevier user license
open archive

Highlights

  • Recovery of eye dominance and acuity are independent in murine amblyopia

  • ngr1 operates in neocortex to limit recovery of eye dominance

  • ngr1 expression by thalamic neurons restricts improvement of acuity

  • Deleting ngr1 after the critical period is sufficient to restore acuity

Summary

Degrading vision by one eye during a developmental critical period yields enduring deficits in both eye dominance and visual acuity. A predominant model is that “reactivating” ocular dominance (OD) plasticity after the critical period is required to improve acuity in amblyopic adults. However, here we demonstrate that plasticity of eye dominance and acuity are independent and restricted by the nogo-66 receptor (ngr1) in distinct neuronal populations. Ngr1 mutant mice display greater excitatory synaptic input onto both inhibitory and excitatory neurons with restoration of normal vision. Deleting ngr1 in excitatory cortical neurons permits recovery of eye dominance but not acuity. Reciprocally, deleting ngr1 in thalamus is insufficient to rectify eye dominance but yields improvement of acuity to normal. Abolishing ngr1 expression in adult mice also promotes recovery of acuity. Together, these findings challenge the notion that mechanisms for OD plasticity contribute to the alterations in circuitry that restore acuity in amblyopia.

Keywords

amblyopia
visual acuity
eye dominance
plasticity
leucine-rich repeat

Cited by (0)

7

Lead Contact