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Critical periods in amblyopia

HENSCH, TAKAO K., QUINLAN, ELIZABETH M.·2018·Visual Neuroscience

DOI 10.1017/s0952523817000219PMC PMC6047524

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Abstract

The shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

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See all 206

Authors: HENSCH, T. K., & QUINLAN, E. M.
Venue: Visual Neuroscience
Publisher: Maximum Academic Press
Published: 2018
Volume: 35
ISSN: 0952-5238
1469-8714
DOI: 10.1017/s0952523817000219
PMC: PMC6047524
Cited by: 206
References: 146
Language: en
Licence: www.cambridge.org/core/terms (unspecified, 105 d)

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Critical periods in amblyopia

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