Lack of CaBP1/Caldendrin or CaBP2 Leads to Altered Ganglion Cell Responses

Calcium-binding proteins (CaBPs) form a subfamily of calmodulin-like proteins that were cloned from the retina. CaBP4 and CaBP5 have been shown to be important for normal visual function. Although CaBP1/caldendrin and CaBP2 have been shown to modulate various targets , it is not known whether they c...

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Published ineNeuro Vol. 3; no. 5; p. ENEURO.0099-16.2016
Main Authors Sinha, Raunak, Lee, Amy, Rieke, Fred, Haeseleer, Françoise
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 01.09.2016
Subjects
Action Potentials
Animals
Calcium-Binding Proteins - deficiency
Calcium-Binding Proteins - genetics
Immunohistochemistry
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Electron
New Research
Patch-Clamp Techniques
Photic Stimulation
Retinal Bipolar Cells - metabolism
Retinal Bipolar Cells - ultrastructure
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - ultrastructure
Synapses - metabolism
Synapses - ultrastructure
Tissue Culture Techniques
Vision, Ocular - physiology
bipolar cells
knockout mice
ganglion cells
retina
light response
calcium-binding proteins
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Summary:Calcium-binding proteins (CaBPs) form a subfamily of calmodulin-like proteins that were cloned from the retina. CaBP4 and CaBP5 have been shown to be important for normal visual function. Although CaBP1/caldendrin and CaBP2 have been shown to modulate various targets , it is not known whether they contribute to the transmission of light responses through the retina. Therefore, we generated mice that lack CaBP2 or CaBP1/caldendrin ( and ) to test whether these CaBPs are essential for normal retinal function. By immunohistochemistry, the overall morphology of and retinas and the number of synaptic ribbons appear normal; transmission electron microscopy shows normal tethered ribbon synapses and synaptic vesicles as in wild-type retinas. However, whole-cell patch clamp recordings showed that light responses of retinal ganglion cells of and mice differ in amplitude and kinetics from those of wild-type mice. We conclude that CaBP1/caldendrin and CaBP2 are not required for normal gross retinal and synapse morphology but are necessary for the proper transmission of light responses through the retina; like other CaBPs, CaBP1/caldendrin and CaBP2 likely act by modulating presynaptic Ca -dependent signaling mechanisms.
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The authors report no conflict of interest.
The research was supported by a University of Washington Royalty Research Fund, University of Washington bridge funding, and National Institutes of Health (NIH) grant R01 EY020850 to F.H.; the Howard Hughes Medical Institute and NIH grant EY11850 to F.R.; NIH grants NS084190 and DC009433 and a Carver Research Program of Excellence to A.L.; and a long-term fellowship by Human Frontier Science Program to R.S.
Author Contributions: R.S., F.R., and F.H. designed and performed research and analyzed the data. A.L. contributed unpublished reagents. All authors contributed to writing and approval of the final manuscript.
ISSN:2373-2822
2373-2822
DOI:10.1523/ENEURO.0099-16.2016