Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCgamma-Modulated GluR1 Phosphorylation in Mice.

Purpose: To determine how visual cortex plasticity changes after monocular deprivation (MD) in mice and whether conventional protein kinase C gamma (cPKCgamma) plays a role in visual cortex plasticity. Methods: cPKCgamma membrane translocation levels were quantified by using immunoblotting to explore the effects of MD on cPKCgamma 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 cPKCgamma on mouse retinal function. Results: Membrane translocation levels of cPKCgamma 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 cPKCgamma+/+ mice after MD. Interestingly, these levels could be downregulated by cPKCgamma knockout compared to cPKCgamma+/++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 cPKCgamma+/+ and cPKCgamma-/- mice with MD. Conclusions: cPKCgamma 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 cPKCgamma-mediated phosphorylation of GluR1 at Ser 831.