The sensitivity of ocular dominance to regulation by monocular deprivation is the canonical model of plasticity confined to a critical period. However, we have previously shown that visual deprivation through dark exposure (DE) reactivates critical period plasticity in adults. Previous work assumed that the elimination of visual input was sufficient to enhance plasticity in the adult mouse visual cortex. In contrast, here we show that light reintroduction (LRx) after DE is responsible for the reactivation of plasticity. LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic ablation of matrix metalloproteinase-9 (MMP-9). LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thalamo-cortical synapses. The reactivation of plasticity by LRx is absent in Mmp9-/- mice, and is rescued by hyaluronidase, an enzyme that degrades core ECM components. The LRx-induced increase in MMP-9 removes constraints on structural and functional plasticity in the mature cortex.
- Elizabeth Quinlan
The NEI had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Animal experimentation: All procedures, under Quinlan lab protocol R-16-30, conformed to the guidelines of the University of Maryland Institutional Animal Care and Use Committee and the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health.
- Sacha B Nelson, Brandeis University, United States
© 2017, Murase et al.
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