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A more recent version of this article appeared on July 1, 2008
 (Investigative Ophthalmology and Visual Science. )
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1720
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Article

Ionic Dysregulatory Phenotyping of Pathologic Retinal Thinning with Manganese-enhanced MRI

Bruce A. Berkowitz 1*, Marius Gradianu 2, Stephen Schafer 2, Ying Jin 2, Andre Porchia 2, Raymond Iezzi 3, and Robin Roberts 2

1 Department of Anatomy & Cell Biology, Wayne State University School of Medicine, 540 East Canfield, Detroit, Michigan, 48201, United States; Ophthalmology, Kresge Eye Institute, Detroit, Michigan, United States
2 Department of Anatomy & Cell Biology, Wayne State University School of Medicine, 540 East Canfield, Detroit, Michigan, 48201, United States
3 Ophthalmology, Kresge Eye Institute, Detroit, Michigan, United States

* To whom correspondence should be addressed. E-mail: baberko{at}med.wayne.edu.


  Abstract

Purpose: To test the hypothesis that manganese-enhanced MRI (MEMRI) provides a sensitive and robust measure of an important retinal ionic dysregulatory phenotype in pathologic retinal thinning. Methods: Four hours post MnCl2 injection i.p., high resolution MEMRI data were collected from over-night dark-adapted male control Sprague Dawley and albino RCS rats before (at development stage P17) and during photoreceptor degeneration (P36 and P57). In separate experiments, control rats, with and without repetitive hypoxic preconditioning, were subjected to high intraocular pressure (100 mm Hg) for 60 min followed by 24 hr or 7 days of reperfusion (e.g., ischemia/reperfusion or I/R). Central retinal thickness and intraretinal ion activity were measured from the MEMRI data. Histology examination was also performed to confirm retinal damage. Results: In two different neurodegenerative models, manganese-enhanced MRI (MEMRI) revealed first time evidence for changes (P < 0.05) in intraretinal ionic dysregulation prior to and during pathologic, but not (P > 0.05) developmental, retinal thinning. This phenotype was significantly altered by a neuroprotective repetitive hypoxic preconditioning protocol. Conclusions: MEMRI and a non-toxic systemic dose of MnCl2 provided an objective non-invasive measure of an ionic deregulatory phenotype which appears useful for improved early diagnosis and treatment prognosis in a range of neurodegenerative diseases and their treatment.

Key Words: retinal degeneration, retinitis pigmentosa, Ca2+ channels






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