Photoreceptor regulated expression of Ca2+/calmodulin-dependent protein kinase II in the mouse retina

被引:21
作者
Liu, LO
Li, GY
McCall, MA
Cooper, NGF [1 ]
机构
[1] Univ Louisville, Sch Med, Dept Ophthalmol & Visual Sci, Louisville, KY 40202 USA
[2] Univ Louisville, Sch Med, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA
[3] Univ Louisville, Sch Med, Dept Psychol & Brain Sci, Louisville, KY 40202 USA
来源
MOLECULAR BRAIN RESEARCH | 2000年 / 82卷 / 1-2期
关键词
CaMKII; photoreceptor; retina; synaptic plasticity; CPEB;
D O I
10.1016/S0169-328X(00)00203-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The objective of this investigation is to determine mechanisms for regulation of retinal calmodulin kinase II (CaMKII). To this end, the expression and activity of CaMKII are examined in the retina of the rdta mouse, in which rod photoreceptors have been genetically ablated [47]. CaMKII levels are compared between rdta mice and the normal, littermate control mice. It is demonstrated that retinal CaMKII protein, enzyme activity and mRNA are significantly increased in response to the genetic ablation of rod photoreceptors. The data indicate that CaMKII expression/activity in amacrine and ganglion cells is negatively regulated by the rod photoreceptor-mediated visual input. The regulation appears to occur primarily at the transcriptional level. It is shown that the cytoplasmic polyadenylation element binding protein (CPEB), a regulatory factor for translation that is known to promote CaMKII alpha translation in dendrites [83], is also present in the mouse retina. However, the polyadenylation-mediated translational control mechanism is not activated in this experimental paradigm. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:150 / 166
页数:17
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