scholarly journals Endogenous opioids as substrates for ethanol intake in the neonatal rat: The impact of prenatal ethanol exposure on the opioid family in the early postnatal period

2015 ◽  
Vol 148 ◽  
pp. 100-110 ◽  
Author(s):  
Kelly Bordner ◽  
Terrence Deak
Keyword(s):  
Postnatal Period ◽  
Ethanol Exposure ◽  
Endogenous Opioids ◽  
Ethanol Intake ◽  
Neonatal Rat ◽  
Early Postnatal Period ◽  
Prenatal Ethanol Exposure ◽  
The Impact

Neurobiology of Fetal Alcohol Spectrum Disorders

2017 ◽  
Author(s):  
Carmen Lopez-Arvizu ◽  
Carmel Bogle ◽  
Harolyn M.E. Belcher
Keyword(s):  
Hormonal Regulation ◽  
Maternal Nutrition ◽  
Fetal Alcohol Spectrum Disorders ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Wide Range ◽  
Spectrum Disorders ◽  
The Impact ◽  
Fetal Alcohol Spectrum

Prenatal exposure to ethanol can result in a wide range of clinical presentations that are grouped under the term “Fetal Alcohol Spectrum Disorders” (FASD). The direct cellular teratogenic effects of ethanol on fetal neurodevelopment include damage to cell survival, proliferation, and migration mechanisms. Dysregulation of neurotransmission and alteration of genetic transcription have also been implicated in the neurotoxic effects of prenatal ethanol exposure. These deleterious events lead to brain volume reduction, corpus callosum dysgenesis, cerebellar, and other neuroanatomical anomalies that have been observed in individuals with FASD. Beyond direct ethanol-induced insults, the impact that ethanol has on maternal nutrition, metabolism, hormonal regulation, and placental physiology also adversely effects fetal development. The complex interactions between numerous neurobiological and psychosocial mechanisms that hinder optimal fetal neurodevelopment are reflected by the heterogeneous clinical presentation of FASD, including impaired growth, dysmorphic facial features, and cognitive and behavioral disorders.

scholarly journals The Impact of Prenatal Ethanol Exposure on Neuroanatomical and Behavioral Development in Mice

2016 ◽  
Vol 40 (1) ◽  
pp. 122-133 ◽  
Author(s):  
Charles W. Abbott ◽  
Olga O. Kozanian ◽  
Joseph Kanaan ◽  
Kara M. Wendel ◽  
Kelly J. Huffman
Keyword(s):  
Behavioral Development ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
The Impact

scholarly journals Prenatal ethanol exposure increases ethanol intake and reduces C-fos expression in infralimbic cortex of adolescent rats

2013 ◽  
Vol 103 (4) ◽  
pp. 842-852 ◽  
Author(s):  
Maria Carolina Fabio ◽  
Samanta M. March ◽  
Juan Carlos Molina ◽  
Michael E. Nizhnikov ◽  
Norman E. Spear ◽  
...  
Keyword(s):  
Ethanol Exposure ◽  
Ethanol Intake ◽  
Prenatal Ethanol Exposure ◽  
Infralimbic Cortex ◽  
Adolescent Rats ◽  
Fos Expression

Effects of prenatal ethanol exposure on choline-induced long-term depression in the hippocampus

2021 ◽  
Author(s):  
Erin L Grafe ◽  
Christine J Fontaine ◽  
Jennifer D Thomas ◽  
Brian R Christie
Keyword(s):  
Choline Chloride ◽  
Hippocampal Slices ◽  
Ethanol Exposure ◽  
Acute Administration ◽  
Prenatal Ethanol Exposure ◽  
Sprague Dawley ◽  
Long Term Depression ◽  
M1 Receptors ◽  
The Impact

Choline is an essential nutrient that is being explored as a nutritional treatment for many neurological disorders. Indeed, choline has already moved to being used in clinical trials for Fetal Alcohol Spectrum Disorders (FASD), and there is increased pressure to better understand its therapeutic mechanism(s) of action. This is particularly true given its potential to directly effect synaptic mechanisms that are believed important for cognitive processes. In the current work we study how the direct application of choline can affect synaptic transmission in hippocampal slices obtained from adolescent (post-natal days 21-28) Sprague-Dawley rats (Rattus norvegicus). The acute administration of choline chloride (2 mM) reliably induced a long-term depression (LTD) of field excitatory postsynaptic potentials (fEPSP) in the DG in vitro. The depression required the involvement of M1-receptors, and the magnitude of the effect was similar in slices obtained from male and female animals. To further study the impact of choline in an animal model of FASD, we examined offspring from dams fed an ethanol-containing diet (35.5% ethanol-derived calories) throughout gestation. In slices from the adolescent animals that experienced prenatal ethanol exposure (PNEE), we found that the choline induced an LTD that uniquely involved the activation of NMDA and M1 receptors. This study provides a novel insight into how choline can modulate hippocampal transmission at the level of the synapse and that it can have unique effects following PNEE.

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

2007 ◽  
Vol 31 (2) ◽  
pp. 181-191 ◽  
Author(s):  
M. Gabriela Chotro ◽  
Carlos Arias ◽  
Giovanni Laviola
Keyword(s):  
Ethanol Exposure ◽  
Ethanol Intake ◽  
Prenatal Ethanol Exposure

Early exposure to environmental enrichment modulates the effects of prenatal ethanol exposure upon opioid gene expression and adolescent ethanol intake

2020 ◽  
Vol 165 ◽  
pp. 107917 ◽  
Author(s):  
Aranza Wille-Bille ◽  
Fabio Bellia ◽  
Ana María Jiménez García ◽  
Roberto Sebastián Miranda-Morales ◽  
Claudio D'Addario ◽  
...  
Keyword(s):  
Gene Expression ◽  
Environmental Enrichment ◽  
Ethanol Exposure ◽  
Ethanol Intake ◽  
Early Exposure ◽  
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.

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