RGD Reference Report - Maternal ethanol exposure induces behavioral deficits through oxidative stress and brain-derived neurotrophic factor interrelation in rat offspring. - Rat Genome Database

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Maternal ethanol exposure induces behavioral deficits through oxidative stress and brain-derived neurotrophic factor interrelation in rat offspring.

Authors: Mahdinia, Rahebeh  Goudarzi, Iran  Lashkarbolouki, Taghi  Elahdadi Salmani, Mahmoud 
Citation: Mahdinia R, etal., Int J Dev Neurosci. 2021 Dec;81(8):717-730. doi: 10.1002/jdn.10148. Epub 2021 Sep 20.
RGD ID: 401959600
Pubmed: PMID:34427953   (View Abstract at PubMed)
DOI: DOI:10.1002/jdn.10148   (Journal Full-text)

Alcohol consumption during pregnancy damages the central nervous system of developing fetus and results in persistent physical and neurobehavioral abnormalities, including learning and memory disorders. The hippocampus which is involved in learning and memory is highly susceptible to the ethanol neurotoxic effects. Oxidative stress is one of the mechanisms in alcohol-induced disorders. Ethanol also interferes with the brain-derived neurotrophic factors (BDNF) expression. Using vitamin E as a potent antioxidant, we studied the possible interrelation between oxidative stress and BDNF on cognition. Ethanol (4 g/kg) and vitamin E (100, 200, and 400 mg/kg) were given to pregnant Wistar rats on first day of gestation (GD) until weaning (28 days). Oxidative stress marker, BDNF expression, and cyclic AMP-response binding-protein (CREB) expression levels were measured on postnatal days (PND) 28. Object location memory (OLM) was evaluated on PND 34. Our results demonstrated that ethanol exposure significantly reduced glutathione peroxidase (GPx) activity, reduced glutathione (GSH), reduced/oxidized glutathione (GSH/GSSG) ratio, and increased superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and carbonyl protein content in the hippocampus. Total BDNF, BDNF mRNA, and CREB expression significantly reduced in the hippocampus by ethanol exposure. Also, ethanol significantly reduced the discrimination index (DI) in the OLM test. In addition, vitamin E administration could reduce oxidative stress, increase significantly BDNF and CREB levels, and improve cognitive dysfunction induced by ethanol exposure. Collectively, results suggest that probably oxidative stress can interrelate with the BDNF system for modulating cognitive function in the ethanol-exposed rat.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Memory Disorders  ISOBdnf (Rattus norvegicus)401959600; 401959600associated with alcohol use disorder more ...RGD 
Memory Disorders  IEP 401959600associated with alcohol use disorder more ...RGD 
Memory Disorders  ISOCreb1 (Rattus norvegicus)401959600; 401959600associated with alcohol use disorder and mRNA:decreased expression:hippocampusRGD 
Memory Disorders  IEP 401959600associated with alcohol use disorder and mRNA:decreased expression:hippocampusRGD 

Objects Annotated

Genes (Rattus norvegicus)
Bdnf  (brain-derived neurotrophic factor)
Creb1  (cAMP responsive element binding protein 1)

Genes (Mus musculus)
Bdnf  (brain derived neurotrophic factor)
Creb1  (cAMP responsive element binding protein 1)

Genes (Homo sapiens)
BDNF  (brain derived neurotrophic factor)
CREB1  (cAMP responsive element binding protein 1)


Additional Information