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Published on: February 15, 2011
Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor
Aaron W McGee1, Yupeng Yang, Quentin S Fischer
1Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA.
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.
Insights
Mutations in the Nogo-66 receptor (NgR) disrupt the normal closure of the critical period for visual cortex plasticity. This leads to prolonged ocular dominance plasticity in mice lacking NgR, impacting neural circuit consolidation.
Area of Science:
- Neuroscience
- Developmental Biology
- Visual System Research
Background:
- Ocular dominance in the visual cortex typically shifts only during a critical developmental window.
- This plasticity is crucial for establishing normal visual processing.
- The cessation of this plasticity normally occurs between 20 and 32 days postnatal in mice.
Purpose of the Study:
- To investigate the role of the Nogo-66 receptor (NgR) in regulating the closure of the critical period for ocular dominance plasticity.
- To understand how NgR signaling influences the consolidation of neural circuits after experience-dependent plasticity.
Main Methods:
- Utilized knockout mice lacking the Nogo-66 receptor (NgR-/- mice).
- Assessed ocular dominance plasticity through monocular deprivation experiments at different postnatal ages (juvenile, 45 days, 120 days).
- Examined the effects of NgR mutations on the timing and duration of visual cortex plasticity.
Main Results:
- NgR-/- mice exhibited normal ocular dominance plasticity during the critical period.
- However, plasticity persisted abnormally in NgR-/- mice beyond the typical critical period.
- Ocular dominance remained plastic in older NgR-/- mice, similar to juvenile stages.
Conclusions:
- Physiological signaling via NgR, involving myelin-derived factors like Nogo, MAG, and OMgp, is essential for consolidating neural circuits established during plasticity.
- Disruption of NgR signaling leads to a failure to cease ocular dominance plasticity.
- These findings suggest NgR plays a critical role in stabilizing visual cortex circuitry and may have implications for understanding recovery after neural injury.
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