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Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
Published on: February 8, 2020
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Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice
Yunxia Zhang1, Tao Fu2, Song Han1
1,.
Investigative Ophthalmology & Visual Science
|April 29, 2020
Summary
Protein kinase C gamma (cPKCγ) activation increases in the visual cortex after monocular deprivation (MD). This protein is crucial for visual cortex plasticity, influencing long-term potentiation (LTP) and synaptic changes.
Area of Science:
- Neuroscience
- Molecular Biology
- Vision Science
Background:
- Monocular deprivation (MD) is a critical period for visual cortex development and plasticity.
- Protein kinase C gamma (cPKCγ) is implicated in synaptic plasticity, but its role in visual cortex plasticity following MD is not fully understood.
Purpose of the Study:
- To investigate changes in visual cortex plasticity after MD in mice.
- To determine the role of conventional protein kinase C gamma (cPKCγ) in visual cortex plasticity following MD.
Main Methods:
- Quantified cPKCγ membrane translocation using immunoblotting.
- Measured field excitatory postsynaptic potential (fEPSP) amplitude via electrophysiology to assess visual cortex plasticity.
- Determined GluR1 phosphorylation at Ser831 using immunoblotting.
- Analyzed retinal function with electroretinography.
Main Results:
- cPKCγ membrane translocation significantly increased in the contralateral visual cortex after MD.
- Long-term potentiation (LTP) and GluR1 phosphorylation at Ser831 were elevated in the contralateral visual cortex of MD mice.
- cPKCγ knockout downregulated these increases, indicating its crucial role.
- MD affected retinal function, evidenced by reduced a-wave and b-wave amplitudes.
Conclusions:
- cPKCγ plays a significant role in visual cortex plasticity after MD.
- Increased LTP in the visual cortex following MD may be mediated by cPKCγ-dependent phosphorylation of GluR1 at Ser831.

