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Literature DB >> 17468749

Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition.

Alessandro Sale¹, José Fernando Maya Vetencourt, Paolo Medini, Maria Cristina Cenni, Laura Baroncelli, Roberto De Pasquale, Lamberto Maffei.

Abstract

Loss of visual acuity caused by abnormal visual experience during development (amblyopia) is an untreatable pathology in adults. We report that environmental enrichment in adult amblyopic rats restored normal visual acuity and ocular dominance. These effects were due to reduced GABAergic inhibition in the visual cortex, accompanied by increased expression of BDNF and reduced density of extracellular-matrix perineuronal nets, and were prevented by enhancement of inhibition through benzodiazepine cortical infusion.

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Year: 2007 PMID： 17468749 DOI： 10.1038/nn1899

Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884

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Cited

200 in total

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Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition.

1. Voluntary physical exercise promotes ocular dominance plasticity in adult mouse primary visual cortex.

2. Reorganization in processing of spectral and temporal input in the rat posterior auditory field induced by environmental enrichment.

3. Experience-dependent expression of NPAS4 regulates plasticity in adult visual cortex.

Review 4. Structural plasticity upon learning: regulation and functions.

5. Obligatory role for the immediate early gene NARP in critical period plasticity.

Review 6. Harnessing activity-dependent plasticity to repair the damaged corticospinal tract in an animal model of cerebral palsy.

7. Adult visual experience promotes recovery of primary visual cortex from long-term monocular deprivation.

8. Neuronal plasticity and antidepressant actions.

9. Neurosteroid allopregnanolone reduces ipsilateral visual cortex potentiation following unilateral optic nerve injury.

Review 10. Neurotrophin regulation of neural circuit development and function.