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. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Chondroitin Sulfate Proteoglycans / metabolism
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Darkness
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Dominance, Ocular / physiology*
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Electrophysiology
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GPI-Linked Proteins
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Gene Targeting
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Mice
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Mice, Inbred C57BL
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Mutation
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Myelin Basic Protein / metabolism
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Myelin Proteins / genetics
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Myelin Proteins / metabolism
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Myelin Proteins / physiology*
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Myelin Sheath / physiology*
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Myelin-Associated Glycoprotein / metabolism
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Neurites / physiology
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Neuronal Plasticity / physiology*
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Neurons / physiology*
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Nogo Proteins
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Nogo Receptor 1
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Photic Stimulation
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / physiology*
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Signal Transduction
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Visual Cortex / cytology
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Visual Cortex / growth & development
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Visual Cortex / physiology*
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gamma-Aminobutyric Acid / physiology
Substances
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Chondroitin Sulfate Proteoglycans
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GPI-Linked Proteins
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Myelin Basic Protein
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Myelin Proteins
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Myelin-Associated Glycoprotein
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Nogo Proteins
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Nogo Receptor 1
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Receptors, Cell Surface
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Rtn4 protein, mouse
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Rtn4r protein, mouse
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gamma-Aminobutyric Acid