Document Detail

Mechanisms for persistent microphthalmia following ethanol exposure during retinal neurogenesis in zebrafish embryos.
MedLine Citation:
PMID:  17640445     Owner:  NLM     Status:  MEDLINE    
The exposure of the developing human embryo to ethanol results in a spectrum of disorders involving multiple organ systems, including the visual system. One common phenotype seen in humans exposed to ethanol in utero is microphthalmia. The objective of this study was to describe the effects of ethanol during retinal neurogenesis in a model organism, the zebrafish, and to pursue the potential mechanisms by which ethanol causes microphthalmia. Zebrafish embryos were exposed to 1% or 1.5% ethanol from 24 to 48 h after fertilization, a period during which the retinal neuroepithelium undergoes rapid proliferation and differentiation to form a laminated structure composed of different retinal cell types. Ethanol exposure resulted in significantly reduced eye size immediately following the treatment, and this microphthalmia persisted through larval development. This reduced eye size could not entirely be accounted for by the accompanying general delay in embryonic development. Retinal cell death was only slightly higher in ethanol-exposed embryos, although cell death in the lens was extensive in some of these embryos, and lenses were significantly reduced in size as compared to those of control embryos. The initiation of retinal neurogenesis was not affected, but the subsequent waves of cell differentiation were markedly reduced. Even cells that were likely generated after ethanol exposure--rod and cone photoreceptors and Müller glia--were delayed in their expression of cell-specific markers by at least 24 h. We conclude that ethanol exposure over the time of retinal neurogenesis resulted in persistent microphthalmia due to a combination of an overall developmental delay, lens abnormalities, and reduced retinal cell differentiation.
Bhavani Kashyap; Logan C Frederickson; Deborah L Stenkamp
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-07-20
Journal Detail:
Title:  Visual neuroscience     Volume:  24     ISSN:  0952-5238     ISO Abbreviation:  Vis. Neurosci.     Publication Date:    2007 May-Jun
Date Detail:
Created Date:  2007-09-07     Completed Date:  2007-11-28     Revised Date:  2014-09-15    
Medline Journal Info:
Nlm Unique ID:  8809466     Medline TA:  Vis Neurosci     Country:  England    
Other Details:
Languages:  eng     Pagination:  409-21     Citation Subset:  IM    
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MeSH Terms
Abnormalities, Drug-Induced
Cell Count / methods
Cell Proliferation / drug effects*
Central Nervous System Depressants / toxicity*
Dose-Response Relationship, Drug
Embryo, Nonmammalian / drug effects*,  pathology
Embryonic Development / drug effects
Ethanol / toxicity*
Eye Proteins / metabolism
Gene Expression Regulation, Developmental / drug effects
Histones / metabolism
Homeodomain Proteins / metabolism
In Situ Nick-End Labeling / methods
Neurons / drug effects*,  physiology
Paired Box Transcription Factors / metabolism
Repressor Proteins / metabolism
Retina / pathology*
Thalamus* / abnormalities,  drug effects,  embryology
Time Factors
Grant Support
P20RR016454/RR/NCRR NIH HHS; R01 EY012146/EY/NEI NIH HHS; R01 EY012146-07/EY/NEI NIH HHS; R01 EY012146-08/EY/NEI NIH HHS; R01EY012146/EY/NEI NIH HHS
Reg. No./Substance:
0/Central Nervous System Depressants; 0/Eye Proteins; 0/Histones; 0/Homeodomain Proteins; 0/PAX6 protein; 0/Paired Box Transcription Factors; 0/Repressor Proteins; 3K9958V90M/Ethanol

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

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