Document Detail


Immunohistochemical evidence of synaptic retraction, cytoarchitectural remodeling, and cell death in the inner retina of the rat model of oygen-induced retinopathy (OIR).
MedLine Citation:
PMID:  21071736     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Postnatal exposure to hyperoxia destroys the plexiform layers of the neonatal rat retina, resulting in significant electroretinographic anomalies. The purpose of this study was to identify the mechanisms at the origin of this loss.
METHODS: Sprague-Dawley (SD) and Long Evans (LE) rats were exposed to hyperoxia from birth to postnatal day (P) 6 or P14 and from P6 to P14, after which rats were euthanatized at P6, P14, or P60.
RESULTS: At P60, synaptophysin staining confirmed the lack of functional synaptic terminals in SD (outer plexiform layer [OPL]) and LE (OPL and inner plexiform layer [IPL]) rats. Uneven staining of ON-bipolar cell terminals with mGluR6 suggests that their loss could play a role in OPL thinning. Protein kinase C(PKC)-α and recoverin (rod and cone ON-bipolar cells, respectively) showed a lack of dendritic terminals in the OPL with disorganized axonal projections in the IPL. Although photoreceptor nuclei appeared intact, a decrease in bassoon staining (synaptic ribbon terminals) suggests limited communication to the inner retina. Findings were significantly more pronounced in LE rats. An increase in TUNEL-positive cells was observed in LE (inner nuclear layer [INL] and outer nuclear layer [ONL]) and SD (INL) rats after P0 to P14 exposure (425.3%, 102.2%, and 146.3% greater than control, respectively [P < 0.05]).
CONCLUSIONS: Results suggest that cell death and synaptic retraction are at the root of OPL thinning. Increased TUNEL-positive cells in the INL confirm that cells die, at least in part, because of apoptosis. These findings propose a previously undescribed mechanism of cell death and synaptic retraction that are likely at the origin of the functional consequences of hyperoxia.
Authors:
Allison Lindsay Dorfman; Nicolás Cuenca; Isabel Pinilla; Sylvain Chemtob; Pierre Lachapelle
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-03-25
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  52     ISSN:  1552-5783     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-28     Completed Date:  2011-05-27     Revised Date:  2013-01-09    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1693-708     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, McGill University-Montreal Children’s Hospital Research Institute, Montreal, Quebec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Apoptosis*
Biological Markers / metabolism
Disease Models, Animal*
Eye Proteins / metabolism
Female
Fluorescent Antibody Technique, Indirect
Humans
Hyperoxia / metabolism*,  pathology
In Situ Nick-End Labeling
Infant, Newborn
Male
Microscopy, Confocal
Neuronal Plasticity / physiology*
Oxygen / toxicity
Presynaptic Terminals / metabolism*
Rats
Rats, Long-Evans
Rats, Sprague-Dawley
Retinal Neurons / physiology*
Retinopathy of Prematurity / metabolism*,  pathology
Grant Support
ID/Acronym/Agency:
MOP-13383//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Eye Proteins; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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