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Imaging Ca2+ Dynamics in Cone Photoreceptor Axon Terminals of the Mouse Retina
Published on: May 6, 2015
Photoreceptor regulated expression of Ca(2+)/calmodulin-dependent protein kinase II in the mouse retina
1Department of Ophthalmology and Visual Sciences, School of Medicine University of Louisville, Louisville, KY 40202, USA.
Abstract:
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 CaMKIIalpha 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.
Insights
Rod photoreceptor loss increases retinal calmodulin kinase II (CaMKII) expression and activity. This suggests visual input normally suppresses CaMKII in amacrine and ganglion cells, primarily at the transcriptional level.
Area of Science:
- Neuroscience
- Molecular Biology
- Retinal Physiology
Background:
- Calmodulin kinase II (CaMKII) plays crucial roles in neuronal function.
- Understanding CaMKII regulation in the retina is vital for comprehending visual processing.
Purpose of the Study:
- To investigate the regulatory mechanisms of retinal CaMKII.
- To determine how the absence of rod photoreceptors affects CaMKII expression and activity.
Main Methods:
- Comparative analysis of CaMKII protein, activity, and mRNA in rdta mice (rod photoreceptor-ablated) versus control mice.
- Examination of the role of cytoplasmic polyadenylation element binding protein (CPEB) in retinal CaMKII regulation.
Main Results:
- Retinal CaMKII protein, enzyme activity, and mRNA levels were significantly elevated in rdta mice.
- Rod photoreceptor ablation leads to increased CaMKII in amacrine and ganglion cells.
- Regulation appears to be primarily transcriptional, not translational via CPEB.
Conclusions:
- Rod photoreceptor-mediated visual input negatively regulates retinal CaMKII expression and activity.
- The primary regulatory mechanism is at the transcriptional level.
- The translational control mechanism involving CPEB is not active in this context.
