Effects of prenatal ethanol exposure on the development of Bergmann glia and astrocytes in the rat cerebellum: An immunohistochemical study

1992 ◽  
Vol 321 (1) ◽  
pp. 19-32 ◽  
Author(s):  
Ashok K. Shetty ◽  
Dwight E. Phillips
Keyword(s):  
Immunohistochemical Study ◽  
Ethanol Exposure ◽  
Bergmann Glia ◽  
Prenatal Ethanol Exposure ◽  
Rat Cerebellum

Effects of acute prenatal ethanol exposure on Bergmann glia cells early postnatal development

1997 ◽  
Vol 746 (1-2) ◽  
pp. 305-308 ◽  
Author(s):  
Esther Pérez-Torrero ◽  
Pilar Durán ◽  
Leticia Granados ◽  
Gabriel Gutiérrez-Ospina ◽  
León Cintra ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Ethanol Exposure ◽  
Bergmann Glia ◽  
Prenatal Ethanol Exposure ◽  
Early Postnatal Development ◽  
Glia Cells

Combined pre- and postnatal ethanol exposure alters the development of bergmann glia in rat cerebellum

1994 ◽  
Vol 12 (7) ◽  
pp. 641-649 ◽  
Author(s):  
Ashok K. Shetty ◽  
Robert C. Burrows ◽  
Kenneth A. Wall ◽  
Dwight E. Phillips
Keyword(s):  
Ethanol Exposure ◽  
Bergmann Glia ◽  
Rat Cerebellum

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

Permanent abnormal response to a glucose load after prenatal ethanol exposure in rats

Alcohol ◽  
1989 ◽  
Vol 6 (6) ◽  
pp. 469-473 ◽  
Author(s):  
Dolores López-Tejero ◽  
Miquel Llobera ◽  
Emilio Herrera
Keyword(s):  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Glucose Load ◽  
Abnormal Response

Prenatal ethanol exposure impairs the conduction delay at the atrioventricular junction in the looping heart

2021 ◽  
Author(s):  
Shan Ling ◽  
Michael W Jenkins ◽  
Michiko Watanabe ◽  
Stephanie M Ford ◽  
Andrew M Rollins
Keyword(s):  
Heart Development ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Heart Defects ◽  
Ethanol Exposure ◽  
Cardiac Conduction ◽  
Conduction Delay ◽  
Prenatal Ethanol Exposure ◽  
Endocardial Cushions ◽  
Atrioventricular Junction

The etiology of ethanol-related congenital heart defects has been the focus of much study, but most research has concentrated on cellular and molecular mechanisms. We have shown with optical coherence tomography (OCT) that ethanol exposure led to increased retrograde flow and smaller atrioventricular (AV) cushions compared to controls. Since AV cushions play a role in patterning the conduction delay at the atrioventricular junction (AVJ), this study aims to investigate whether ethanol exposure alters the AVJ conduction in early looping hearts and whether this alteration is related to the decreased cushion size. Quail embryos were exposed to a single dose of ethanol at gastrulation, and Hamburger-Hamilton stage 19 - 20 hearts were dissected for imaging. Cardiac conduction was measured using an optical mapping microscope and we imaged the endocardial cushions using OCT. Our results showed that, compared with controls, ethanol-exposed embryos exhibited abnormally fast AVJ conduction and reduced cushion size. However, this increased conduction velocity (CV) did not strictly correlate with decreased cushion volume and thickness. By matching the CV map to the cushion size map, we found that the slowest conduction location was consistently at the atrial side of the AVJ, which had the thinner cushions, not at the thickest cushion location at the ventricular side as expected. Our findings reveal regional differences in the AVJ myocardium even at this early stage in heart development. These findings reveal the early steps leading to the heterogeneity and complexity of conduction at the mature AVJ, a site where arrhythmias can be initiated.

Prenatal ethanol exposure potentiates isolation-induced ethanol consumption in young adult rats

Alcohol ◽  
2019 ◽  
Vol 75 ◽  
pp. 39-46 ◽  
Author(s):  
Macarena Soledad Fernández ◽  
Jorge Carrizo ◽  
Wladimir Plaza ◽  
Paola Haeger ◽  
Ricardo Marcos Pautassi
Keyword(s):  
Young Adult ◽  
Ethanol Consumption ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Adult Rats
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