scholarly journals Inside Cover: In‐vivo hemodynamic imaging of acute prenatal ethanol exposure in fetal brain by photoacoustic tomography (J. Biophotonics 5/2020)

2020 ◽  
Vol 13 (5) ◽  
Author(s):  
Tianqi Shan ◽  
Yuan Zhao ◽  
Shixie Jiang ◽  
Huabei Jiang
Keyword(s):  
Fetal Brain ◽  
Ethanol Exposure ◽  
Photoacoustic Tomography ◽  
Prenatal Ethanol Exposure

Ethanol neurobehavioural teratogenesis and the role of L-glutamate in the fetal hippocampus

1995 ◽  
Vol 73 (9) ◽  
pp. 1209-1223 ◽  
Author(s):  
James D. Reynolds ◽  
James F. Brien
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Neuronal Development ◽  
Excitatory Amino Acid ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Current State ◽  
Developing Neurons

The purpose of this article is to review the current state of knowledge of ethanol neurobehavioural teratogenesis and its postulated mechanisms. The review comprises an examination of ethanol teratogenesis in the human, including the fetal alcohol syndrome, and in experimental animals. Several current proposed mechanisms of ethanol neurobehavioural teratogenesis are critically assessed, including the role of acetaldehyde as the proximate metabolite of ethanol; fetal hypoxia; placental dysfunction; fetal prostaglandin metabolism; and action of ethanol on developing neurons in the fetal brain, including the hippocampus, one of ethanol's main target sites. The effect of ethanol on the release of L-glutamate, an excitatory amino acid neurotransmitter, in the fetal hippocampus is described, and the role of L-glutamate in ethanol teratogenesis involving the hippocampus is discussed. A novel mechanism for abnormal neuronal development in the fetal hippocampus produced by prenatal ethanol exposure is presented, and future experiments to test this hypothesis are proposed.Key words: ethanol neurobehavioural teratogenesis, fetal alcohol syndrome, hippocampus, L-glutamate.

DHA supplementation during prenatal ethanol exposure alters the expression of fetal rat liver genes involved in oxidative stress regulation

2019 ◽  
Vol 44 (7) ◽  
pp. 744-750 ◽  
Author(s):  
Bradley A. Feltham ◽  
Xavier L. Louis ◽  
Fatemeh Ramezani Kapourchali ◽  
Michael N.A. Eskin ◽  
Miyoung Suh
Keyword(s):  
Messenger Rna ◽  
Fetal Alcohol Spectrum Disorders ◽  
Fetal Liver ◽  
Fetal Brain ◽  
Signs And Symptoms ◽  
Liver Weight ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Sprague Dawley ◽  
Gene Expressions

Prenatal ethanol (EtOH) exposure is known to induce adverse effects on fetal brain development. Docosahexaenoic acid (DHA) has been shown to alleviate these effects by up-regulating antioxidant mechanisms in the brain. The liver is the first organ to receive enriched blood after placental transport. Therefore, it could be negatively affected by EtOH, but no studies have assessed the effects of DHA on fetal liver. This study examined the effects of maternal DHA intake on DHA status and gene expression of key enzymes of the glutathione antioxidant system in the fetal liver after prenatal EtOH exposure. Pregnant Sprague–Dawley dams were intubated with EtOH for the first 10 days of pregnancy, while being fed a control or DHA-supplemented diet. Fetal livers were collected at gestational day 20, and free fatty acids and phospholipid profile, as well as glutathione reductase (GR) and glutathione peroxidase-1 (GPx1) gene expressions, were assessed. Prenatal EtOH exposure increased fetal liver weight, whereas maternal DHA supplementation decreased fetal liver weight. DHA supplementation increased fetal liver free fatty acid and phospholipid DHA independently of EtOH. GR and GPx1 messenger RNA (mRNA) expressions were significantly increased and decreased, respectively, in the EtOH-exposed group compared with all other groups. Providing DHA normalized GR and GPx1 mRNA expression to control levels. This study shows that maternal DHA supplementation alters the expression of fetal liver genes involved in the glutathione antioxidative system during prenatal EtOH exposure. The fetal liver may play an important role in mitigating the signs and symptoms of fetal alcohol spectrum disorders in affected offspring.

scholarly journals Dose-response analysis of microvasculature changes in the murine fetal brain and the maternal extremities due to prenatal ethanol exposure

2020 ◽  
Vol 25 (12) ◽  
Author(s):  
Raksha Raghunathan ◽  
Chih-Hao Liu ◽  
Amur Kouka ◽  
Manmohan Singh ◽  
Rajesh C. Miranda ◽  
...  
Keyword(s):  
Dose Response ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Response Analysis ◽  
Prenatal Ethanol Exposure

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.

scholarly journals Maternal Ethanol Exposure Acutely Elevates Src Family Kinase Activity in the Fetal Cortex

2021 ◽  
Author(s):  
Dandan Wang ◽  
Brian W. Howell ◽  
Eric C. Olson
Keyword(s):  
Tyrosine Phosphorylation ◽  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Src Family Kinase ◽  
Cortical Cells ◽  
Signaling Systems ◽  
Sustained Reduction ◽  
Reelin Signaling

AbstractFetal alcohol syndrome (FAS) is characterized by disrupted fetal brain development and postnatal cognitive impairment. The targets of alcohol are diverse, and it is not clear whether there are common underlying molecular mechanisms producing these disruptions. Prior work established that acute ethanol exposure causes a transient increase in tyrosine phosphorylation of multiple proteins in cultured embryonic cortical cells. In this study, we show that a similar tyrosine phosphorylation transient occurs in the fetal brain after maternal dosing with ethanol. Using phospho-specific antibodies and immunohistochemistry, we mapped regions of highest tyrosine phosphorylation in the fetal cerebral cortex and found that areas of dendritic and axonal growth showed elevated tyrosine phosphorylation 10 min after maternal ethanol exposure. These were also areas of Src expression and Src family kinase (SFK) activation loop phosphorylation (pY416) expression. Importantly, maternal pretreatment with the SFK inhibitor dasatinib completely prevents both the pY416 increase and the tyrosine phosphorylation response. The phosphorylation response was observed in the perisomatic region and neurites of immature migrating and differentiating primary neurons. Importantly, the initial phosphotyrosine transient (~ 30 min) targets both Src and Dab1, two critical elements in Reelin signaling, a pathway required for normal cortical development. This initial phosphorylation response is followed by sustained reduction in Ser3 phosphorylation of n-cofilin, a critical actin severing protein and an identified downstream effector of Reelin signaling. This biochemical disruption is associated with sustained reduction of F-actin content and disrupted Golgi apparatus morphology in developing cortical neurons. The finding outlines a model in which the initial activation of SFKs by ethanol has the potential to disrupt multiple developmentally important signaling systems for several hours after maternal exposure.

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

scholarly journals The Inferior Colliculus in Alcoholism and Beyond

2020 ◽  
Vol 14 ◽  
Author(s):  
Tanuja Bordia ◽  
Natalie M. Zahr
Keyword(s):  
Inferior Colliculus ◽  
Ethanol Exposure ◽  
Ethanol Withdrawal ◽  
Hypoxic Injury ◽  
Auditory Gating ◽  
Korsakoff Syndrome ◽  
Altered Metabolism ◽  
Magnetic Resonance Imaging Mri ◽  
Inferior Colliculi

Post-mortem neuropathological and in vivo neuroimaging methods have demonstrated the vulnerability of the inferior colliculus to the sequelae of thiamine deficiency as occurs in Wernicke-Korsakoff Syndrome (WKS). A rich literature in animal models ranging from mice to monkeys—including our neuroimaging studies in rats—has shown involvement of the inferior colliculi in the neural response to thiamine depletion, frequently accomplished with pyrithiamine, an inhibitor of thiamine metabolism. In uncomplicated alcoholism (i.e., absent diagnosable neurological concomitants), the literature citing involvement of the inferior colliculus is scarce, has nearly all been accomplished in preclinical models, and is predominately discussed in the context of ethanol withdrawal. Our recent work using novel, voxel-based analysis of structural Magnetic Resonance Imaging (MRI) has demonstrated significant, persistent shrinkage of the inferior colliculus using acute and chronic ethanol exposure paradigms in two strains of rats. We speculate that these consistent findings should be considered from the perspective of the inferior colliculi having a relatively high CNS metabolic rate. As such, they are especially vulnerable to hypoxic injury and may be provide a common anatomical link among a variety of disparate insults. An argument will be made that the inferior colliculi have functions, possibly related to auditory gating, necessary for awareness of the external environment. Multimodal imaging including diffusion methods to provide more accurate in vivo visualization and quantification of the inferior colliculi may clarify the roles of brain stem nuclei such as the inferior colliculi in alcoholism and other neuropathologies marked by altered metabolism.

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