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

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机构: [1]Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China [2]Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China
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关键词: visual cortex plasticity monocular deprivation long-term potentiation cPKC gamma

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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 (cPKC gamma) plays a role in visual cortex plasticity. METHODS. cPKC gamma membrane translocation levels were quantified by using immunoblotting to explore the effects of MD on cPKC gamma 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 cPKC gamma on mouse retinal function. RESULTS. Membrane translocation levels of cPKC gamma 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 cPKC gamma(+/+) mice after MD. Interestingly, these levels could be downregulated by cPKC gamma knockout compared to cPKC gamma(+/+)+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 cPKC gamma(+/+) and cPKC gamma(-/-) mice with MD. CONCLUSIONS. cPKC gamma 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 cPKC gamma-mediated phosphorylation of GluR1 at Ser 831.

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出版当年[2019]版:
大类 | 2 区 医学
小类 | 2 区 眼科学
最新[2023]版:
大类 | 2 区 医学
小类 | 2 区 眼科学
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出版当年[2018]版:
Q1 OPHTHALMOLOGY
最新[2023]版:
Q1 OPHTHALMOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2018版] 出版当年五年平均 出版前一年[2017版] 出版后一年[2019版]

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第一作者机构: [1]Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China
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通讯机构: [1]Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China [2]Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China [*1]Beijing Tongren Eye Center, Capital Medical University, Beijing 100730, China [*2]Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China
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