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Reversible blockade of experience-dependent plasticity by calcineurin in mouse visual cortex
Yupeng Yang1, Quentin S Fischer, Ying Zhang
1Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut 06520, USA. yuyang@aecom.yu.edu
Nature Neuroscience
|May 10, 2005
Summary
Calcineurin, a brain phosphatase, regulates visual cortex plasticity. Increased calcineurin activity in mice prevents visual cortex changes after monocular deprivation, highlighting the kinase-phosphatase balance in neural plasticity.
Area of Science:
- Neuroscience
- Molecular Biology
- Synaptic Plasticity
Background:
- Protein kinases are known regulators of visual cortex plasticity.
- The role of serine/threonine protein phosphatases in this process remains unclear.
- Calcineurin, a Ca2+/calmodulin-activated phosphatase, constrains synaptic plasticity and memory in the hippocampus.
Purpose of the Study:
- To investigate the role of calcineurin in ocular dominance plasticity in the visual cortex.
- To determine if calcineurin activity influences visual cortex responsiveness following monocular deprivation.
Main Methods:
- Utilized transgenic mice with inducible forebrain neuron overexpression of calcineurin.
- Administered monocular deprivation to mice to study visual cortex plasticity.
- Assessed changes in visual cortex responsiveness.
Main Results:
- A transient increase in calcineurin activity was observed to inhibit the shift in visual cortex responsiveness after monocular deprivation.
- This inhibitory effect of calcineurin was found to be reversible.
- Demonstrated calcineurin's involvement in ocular dominance plasticity.
Conclusions:
- Calcineurin plays a significant role in regulating ocular dominance plasticity.
- The balance between protein kinases and phosphatases is crucial for visual cortex plasticity.
- These findings suggest calcineurin as a potential target for modulating visual cortex function.