Maternal Methyl-Enriched Diet Increases DNMT1, HCN1, and TH Gene Expression and Suppresses Absence Seizures and Comorbid Depression in Offspring of WAG/Rij Rats

Bibliographic Details
Title: Maternal Methyl-Enriched Diet Increases DNMT1, HCN1, and TH Gene Expression and Suppresses Absence Seizures and Comorbid Depression in Offspring of WAG/Rij Rats
Authors: Karine Yu. Sarkisova, Ekaterina A. Fedosova, Alla B. Shatskova, Margarita M. Rudenok, Vera A. Stanishevskaya, Petr A. Slominsky
Source: Diagnostics, Vol 13, Iss 3, p 398 (2023)
Publisher Information: MDPI AG, 2023.
Publication Year: 2023
Collection: LCC:Medicine (General)
Subject Terms: absence epilepsy, animal model, depression-like comorbidity, maternal methyl-enriched diet, gene expression, WAG/Rij rat, Medicine (General), R5-920
More Details: The reduced expression of the HCN1 ion channel in the somatosensory cortex (SSC) and mesolimbic dopamine deficiency are thought to be associated with the genesis of spike-wave discharges (SWDs) and comorbid depression in the WAG/Rij rat model of absence epilepsy. This study aimed to investigate whether the maternal methyl-enriched diet (MED), which affects DNA methylation, can alter DNMT1, HCN1, and TH gene expression and modify absence seizures and comorbid depression in WAG/Rij offspring. WAG/Rij mothers were fed MED (choline, betaine, folic acid, vitamin B12, L-methionine, zinc) or a control diet for a week before mating, during pregnancy, and for a week after parturition. MED caused sustained suppression of SWDs and symptoms of comorbid depression in the offspring. Disease-modifying effects of MED were associated with increased expression of the DNMT1 and HCN1 genes in the SSC and hippocampus, as well as DNMT1, HCN1, and TH genes in the nucleus accumbens. No changes in gene expression were detected in the hypothalamus. The results indicate that maternal MED can suppress the genetic absence epilepsy and comorbid depression in offspring. Increased expression of the DNMT1, HCN1, and TH genes is suggested to be a molecular mechanism of this beneficial phenotypic effect.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2075-4418
Relation: https://www.mdpi.com/2075-4418/13/3/398; https://doaj.org/toc/2075-4418
DOI: 10.3390/diagnostics13030398
Access URL: https://doaj.org/article/4a08d873bfe24d65bd60fee5b5e12fb2
Accession Number: edsdoj.4a08d873bfe24d65bd60fee5b5e12fb2
Database: Directory of Open Access Journals
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More Details
ISSN:20754418
DOI:10.3390/diagnostics13030398
Published in:Diagnostics
Language:English