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J Neurosci. 2014 Aug 27;34(35):11631-40. doi: 10.1523/JNEUROSCI.0545-14.2014.

Plasticity of binocularity and visual acuity are differentially limited by nogo receptor.

Author information

1
Developmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, California 90027.
2
Developmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, California 90027, Centre for Biosystems, Neuroscience, and Nanotechnology, Department of Electronic Engineering, City University of Hong Kong, Kowloon, Hong Kong SAR, China, and.
3
Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona 85004.
4
Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona 85004 sqiu@email.arizona.edu amcgee@usc.edu.
5
Developmental Neuroscience Program, Saban Research Institute, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, California 90027, sqiu@email.arizona.edu amcgee@usc.edu.

Abstract

The closure of developmental critical periods consolidates neural circuitry but also limits recovery from early abnormal sensory experience. Degrading vision by one eye throughout a critical period both perturbs ocular dominance (OD) in primary visual cortex and impairs visual acuity permanently. Yet understanding how binocularity and visual acuity interrelate has proven elusive. Here we demonstrate the plasticity of binocularity and acuity are separable and differentially regulated by the neuronal nogo receptor 1 (NgR1). Mice lacking NgR1 display developmental OD plasticity as adults and their visual acuity spontaneously improves after prolonged monocular deprivation. Restricting deletion of NgR1 to either cortical interneurons or a subclass of parvalbumin (PV)-positive interneurons alters intralaminar synaptic connectivity in visual cortex and prevents closure of the critical period for OD plasticity. However, loss of NgR1 in PV neurons does not rescue deficits in acuity induced by chronic visual deprivation. Thus, NgR1 functions with PV interneurons to limit plasticity of binocularity, but its expression is required more extensively within brain circuitry to limit improvement of visual acuity following chronic deprivation.

KEYWORDS:

Cre recombinase; mice; nogo receptor; ocular dominance plasticity; parvalbumin; visual acuity

PMID:
25164659
PMCID:
PMC4145169
DOI:
10.1523/JNEUROSCI.0545-14.2014
[Indexed for MEDLINE]
Free PMC Article

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