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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Berkowitz, Bruce A. Craft, Cheryl Mae Surmeier, D. James Roberts, Robin Murphy, Geoffrey G. |
| Description | Country affiliation: United States Author Affiliation: Berkowitz BA ( Department of Anatomy and Cell Biology Wayne State University School of Medicine, Detroit, Michigan, United States 2Department of Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan, United States.); Murphy GG ( University of Michigan Medical School, Molecular Behavioral Neuroscience Institute, Molecular and Integrative Physiology, Ann Arbor, Michigan, United States.); Craft CM ( Mary D. Allen Laboratory for Vision Research, USC Eye Institute, and Department of Ophthalmology and Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, Los Angeles, California, United States.); Surmeier DJ ( Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.); Roberts R ( Department of Anatomy and Cell Biology Wayne State University School of Medicine, Detroit, Michigan, United States.) |
| Abstract | PURPOSE: To test the hypothesis that horizontal cell (HC) inhibitory signaling controls the degree to which rod cell membranes are depolarized as measured by the extent to which L-type calcium channels (LTCCs) are open in complete darkness in the mouse retina in vivo. METHODS: Dark-adapted wild-type (wt), CACNA1F (Ca(v)1.4(-/-)), arrestin-1 (Arr1(-/-)), and CACNA1D (Ca(v)1.3(-/-)) C57Bl/6 mice were studied. Manganese-enhanced MRI (MEMRI) evaluated the extent that rod LTCCs are open as an index of loss of HC inhibitory signaling. Subgroups were pretreated with D-cis-diltiazem (DIL) at a dose that specifically antagonizes Ca(v)1.2 channels in vivo. RESULTS: Knockout mice predicted to have impaired HC inhibitory signaling (Ca(v)1.4(-/-) or Arr1(-/-)) exhibited greater than normal rod manganese uptake; inner retinal uptake was also supernormal. Genetically knocking out a closely associated gene not expected to impact HC inhibitory signaling (CACNA1D) did not generate this phenotype. The Arr1(-/-) mice exhibited the largest rod uptake of manganese. Manganese-enhanced MRI of DIL-treated Arr1(-/-) mice suggested a greater number of operant LTCC subtypes (i.e., Ca(v)1.2, 1.3, and 1.4) in rods and inner retina than that in DIL-treated Ca(v)1.4(-/-) mice (i.e., Ca(v)1.3). The Ca(v)1.3(-/-) + DIL-treated mice exhibited evidence for a compensatory contribution from Ca(v)1.2 LTCCs. CONCLUSIONS: The data suggest that loss of HC inhibitory signaling is the proximate cause leading to maximally open LTCCs in rods, and possibly inner retinal cells, in mice in total darkness in vivo, regardless of compensatory changes in LTCC subtype manifested in the mutant mice. |
| ISSN | 01460404 |
| e-ISSN | 15525783 |
| DOI | 10.1167/iovs.15-16581 |
| Journal | Investigative Opthalmology & Visual Science |
| Issue Number | 5 |
| Volume Number | 56 |
| Language | English |
| Publisher | Association for Research in Vision and Ophthalmology |
| Publisher Date | 2015-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Calcium Channels, L-type Metabolism Dark Adaptation Physiology Manganese Retina Retinal Horizontal Cells Signal Transduction Genetics Animals Arrestin Calcium Channel Blockers Pharmacology Calcium Channels Diltiazem Magnetic Resonance Imaging Mice Mice, Inbred C57bl Mice, Knockout Nystagmus, Optokinetic Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Ophthalmology Sensory Systems Cellular and Molecular Neuroscience |
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