Experience-Driven Plasticity of Visual Cortex Limited by Myelin and Nogo Receptor

McGee, Aaron W.; Yang, Yupeng; Fischer, Quentin S.; Daw, Nigel W.; Strittmatter, Stephen M.

doi:10.1126/science.1114362

Cited by 555 publications

(555 citation statements)

References 38 publications

(24 reference statements)

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“…Enzymatic digestion of CSPGS has been shown to restore visual cortical plasticity in adult rats (Pizzorusso et al 2002) and to reverse the effects of long-term monocular deprivation in combination with reverse occlusion (Pizzorusso et al 2006). In NgR K/K knockout mice, the critical period is extended into adulthood (McGee et al 2005), implying that blockade of the Nogo/NgR pathway may be a way to enhance visual cortical plasticity into adulthood.…”

Section: The Present and Potential Future Impact Of Work On Animal Momentioning

confidence: 99%

Neural mechanisms of recovery following early visual deprivation

Mitchell

Sengpiel

2008

Phil. Trans. R. Soc. B

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Natural patterned early visual input is essential for the normal development of the central visual pathways and the visual capacities they sustain. Without visual input, the functional development of the visual system stalls not far from the state at birth, and if input is distorted or biased the visual system develops in an abnormal fashion resulting in specific visual deficits. Monocular deprivation, an extreme form of biased exposure, results in large anatomical and physiological changes in terms of territory innervated by the two eyes in primary visual cortex (V1) and to a loss of vision in the deprived eye reminiscent of that in human deprivation amblyopia. We review work that points to a special role for binocular visual input in the development of V1 and vision. Our unique approach has been to provide animals with mixed visual input each day, which consists of episodes of normal and biased (monocular) exposures. Short periods of concordant binocular input, if continuous, can offset much longer episodes of monocular deprivation to allow normal development of V1 and prevent amblyopia. Studies of animal models of patching therapy for amblyopia reveal that the benefits are both heightened and prolonged by daily episodes of binocular exposure.

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Section: The Present and Potential Future Impact Of Work On Animal Momentioning

confidence: 99%

Neural mechanisms of recovery following early visual deprivation

Mitchell

Sengpiel

2008

Phil. Trans. R. Soc. B

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“…Mice lacking a function gene for NogoA or NgR1 exhibit ocular dominance plasticity as adults, well beyond the end of the critical period [72]. Similarly, removal of CSPG GAGs by repeated injection of ChABC proximal to the visual cortex partially reactivates ocular dominance plasticity [73].…”

Section: Experience-dependent Responses: Role Of Mais and Cspgsmentioning

confidence: 99%

Axonal growth therapeutics: regeneration or sprouting or plasticity?

Cafferty

McGee

Strittmatter

2008

Trends in Neurosciences

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108

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Loss of function after neurological injury frequently occurs through the interruption of axonal connectivity, rather than through cell loss. Functional deficits persist because a multitude of inhibitory factors in degenerating myelin and astroglial scar prevent axonal growth in the adult brain and spinal cord. Given the high clinical significance of achieving functional recovery through axonal growth, substantial research effort has been, and will be, devoted toward this desirable goal. Unfortunately, the labels commonly used in the literature to categorize post-injury axonal anatomy might hinder advancement. In this article, we present an argument for the importance of developing precise terms that describe axonal growth in terms of the inciting event, the distance of axonal extension and the timing of axonal growth. The phenotypes produced by molecular interventions that overcome astroglial scar or myelin-associated inhibitors are reframed and discussed in this context.

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“…With the closing of the visual critical period, cortical myelin matures and myelin associated inhibitors including NogoA, myelinassociated glycoprotein (MAG), and oligodendrocyte-myelinglycopretein (OMgp) are expressed and act upon a common Nogo receptor NgR, which is involved in limiting plasticity (Akbik et al, 2012). NgR knockout mice display prolonged visual plasticity, suggesting its requirement for closure of the critical period (McGee et al, 2005).…”

Section: Regulation Of Critical Period Plasticity Within the Visual Smentioning

confidence: 99%

Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

Hartley

Lee

2014

Neuropsychopharmacol

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At specific maturational stages, neural circuits enter sensitive periods of heightened plasticity, during which the development of both brain and behavior are highly receptive to particular experiential information. A relatively advanced understanding of the regulatory mechanisms governing the initiation, closure, and reinstatement of sensitive period plasticity has emerged from extensive research examining the development of the visual system. In this article, we discuss a large body of work characterizing the pronounced nonlinear changes in fear learning and extinction that occur from childhood through adulthood, and their underlying neural substrates. We draw upon the model of sensitive period regulation within the visual system, and present burgeoning evidence suggesting that parallel mechanisms may regulate the qualitative changes in fear learning across development.

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Experience-Driven Plasticity of Visual Cortex Limited by Myelin and Nogo Receptor

Abstract: Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity.

Cited by 555 publications

References 38 publications

Neural mechanisms of recovery following early visual deprivation

Neural mechanisms of recovery following early visual deprivation

Axonal growth therapeutics: regeneration or sprouting or plasticity?

Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

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