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Updated: Dec 23, 2025
Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
Published on: February 8, 2020
Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice
Yunxia Zhang1, Tao Fu2, Song Han1
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Purpose:
To determine how visual cortex plasticity changes after monocular deprivation (MD) in mice and whether conventional protein kinase C gamma (cPKCγ) plays a role in visual cortex plasticity.
Methods:
cPKCγ membrane translocation levels were quantified by using immunoblotting to explore the effects of MD on cPKCγ activation. Electrophysiology was used to record field excitatory postsynaptic potential (fEPSP) amplitude with the goal of observing changes in visual cortex plasticity after MD. Immunoblotting was also used to determine the phosphorylation levels of GluR1 at Ser831. Light transmission was analyzed using electroretinography to examine the effects of MD and cPKCγ on mouse retinal function.
Results:
Membrane translocation levels of cPKCγ significantly increased in the contralateral visual cortex of MD mice compared to wild-type (WT) mice (P < 0.001). In the contralateral visual cortex, long-term potentiation (LTP) and the phosphorylation levels of GluR1 at Ser 831 were increased in cPKCγ+/+ mice after MD. Interestingly, these levels could be downregulated by cPKCγ knockout compared to cPKCγ+/++MD mice (P < 0.001). Compared to the right eyes of WT mice, the amplitudes of a-waves and b-waves declined in deprived right eyes of mice after MD (P < 0.001). There were no significant differences when comparing cPKCγ+/+ and cPKCγ-/- mice with MD.
Conclusions:
cPKCγ participates in the plasticity of the visual cortex after MD, which is characterized by increased LTP in the contralateral visual cortex, which may be a result of cPKCγ-mediated phosphorylation of GluR1 at Ser 831.
Insights
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.
