Evaluation of TRPM2 Channel‐Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels
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Le résumé fourni par la source
Fetal alcohol syndrome (FAS) can occur because of high amount of alcohol intake during pregnancy and is characterized by both physical and neurological problems. Children diagnosed with FAS have difficulties in learning, memory, and coordination. Hippocampus has a major role in memory and learning. We aimed to determine whether alcohol exposure during pregnancy had any effect on offspring by evaluating learning ability as well as oxidative stress and autophagy in the hippocampus and cortex tissues of litters. Attention was also paid to sex differences. To do so, TRPM2, Beclin1, p62, LC3B, IBA1, parvalbumin, GAD65, and mGluR5 expression levels were evaluated by immunohistochemistry. Lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels, as well as total oxidant (TOS) and total antioxidant (TAS) status were determined by ELISA. Learning experiments were evaluated by the Morris water maze (MWM) test. Our findings demonstrated that IBA1, LC3B, GAD65, and mGluR5 expression levels were higher in female rats of the chronic alcohol exposure (CAE) model. Our IHC results revealed that TRPM2 expression levels were significantly increased in both males and females in the CAE group. Likewise, TAS was lower, and TOS was higher in CAE animals. Moreover, MWM outcomes supported a learning deficiency in CAE litters compared to controls and indicated that female offspring outperformed males in learning experiments. Therefore, our results revealed the detrimental effects of alcohol exposure during pregnancy on autophagy signaling in the hippocampus and cortex tissue of litters, which could affect the learning ability of animals.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé, mais le titre doit être comparé manuellement.
- Titre Crossref
- Evaluation of <scp>TRPM2</scp> Channel‐Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels
- Date Crossref
- 10/10/2024
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Karamanoğlu Mehmetbey University Department of Biophysics pays non établi dans la noticeUniversité ou école supérieure
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Yozgat Bozok Üniversitesi pays non établi dans la noticeUniversité ou école supérieure
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Universidad CES pays non établi dans la noticeUniversité ou école supérieure
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Afyonkarahisar Sağlık Bilimleri Üniversitesi pays non établi dans la noticeUniversité ou école supérieure
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Sivas Cumhuriyet Üniversitesi pays non établi dans la noticeUniversité ou école supérieure
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Universidad de Extremadura pays non établi dans la noticeUniversité ou école supérieure
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School of Medicine Yozgat Bozok University Yozgat Türkiye Department of Histology and Embryology pays non établi dans la noticeUniversité ou école supérieure
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School of Medicine Afyonkarahisar Health Sciences University Afyonkarahisar Türkiye Department of Medical Biology pays non établi dans la noticeUniversité ou école supérieure
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School of Medicine Sivas Cumhuriyet University Sivas Türkiye Department of Physiology pays non établi dans la noticeUniversité ou école supérieure
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Department of Pharmacology and Toxicology School of Veterinary Medicine Sivas Türkiye pays non établi dans la noticeUniversité ou école supérieure
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Faculty of Science University of Extremadura Badajoz Spain Department of Physiology pays non établi dans la noticeUniversité ou école supérieure
Department of Biophysics — Karamanoğlu Mehmetbey University, Yozgat Bozok Üniversitesi et Universidad CES, avec 8 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.