Maternal Methyl-Enriched Diet Increases Dopaminergic Tone of the Mesolimbic Brain System in Adult Offspring of WAG/Rij Rats
- PMID: 36301422
- DOI: 10.1134/S001249662205012X
Maternal Methyl-Enriched Diet Increases Dopaminergic Tone of the Mesolimbic Brain System in Adult Offspring of WAG/Rij Rats
Abstract
The aim of this study is to find out whether maternal methyl-enriched diet affects the content of monoamines and their metabolites in brain structures of adult WAG/Rij offspring. It has been shown for the first time that maternal methyl-enriched diet (choline, betaine, folic acid, vitamin B12, L-methionine, zink) during the perinatal period increases dopaminergic tone of the mesolimbic brain system in adult offspring of WAG/Rij rats, which is accompanied by the suppression of the symptoms of genetic absence epilepsy and comorbid depression. Results suggest that maternal methyl-enriched diet during the perinatal period may be served as a new therapeutic strategy to prevent the development of a hypofunction of the mesolimbic dopaminergic brain system and associated genetic absence epilepsy and comorbid depression in offspring.
Keywords: absence epilepsy; brain monoamines; comorbid depression; genetic model; maternal methyl-enriched diet; offspring.
© 2022. Pleiades Publishing, Ltd.
Similar articles
-
Maternal Methyl-Enriched Diet Increases DNMT1, HCN1, and TH Gene Expression and Suppresses Absence Seizures and Comorbid Depression in Offspring of WAG/Rij Rats.Diagnostics (Basel). 2023 Jan 21;13(3):398. doi: 10.3390/diagnostics13030398. Diagnostics (Basel). 2023. PMID: 36766503 Free PMC article.
-
Gender-Dependent Effect of Maternal Methyl-Enriched Diet on the Expression of Genetic Absence Epilepsy and Comorbid Depression in Adult Offspring of WAG/Rij Rats.Dokl Biol Sci. 2020 Sep;494(1):244-247. doi: 10.1134/S0012496620050075. Epub 2020 Oct 20. Dokl Biol Sci. 2020. PMID: 33083882
-
Maternal care exerts disease-modifying effects on genetic absence epilepsy and comorbid depression.Genes Brain Behav. 2018 Sep;17(7):e12477. doi: 10.1111/gbb.12477. Epub 2018 Apr 30. Genes Brain Behav. 2018. PMID: 29604188
-
The WAG/Rij strain: a genetic animal model of absence epilepsy with comorbidity of depression [corrected].Prog Neuropsychopharmacol Biol Psychiatry. 2011 Jun 1;35(4):854-76. doi: 10.1016/j.pnpbp.2010.11.010. Epub 2010 Nov 17. Prog Neuropsychopharmacol Biol Psychiatry. 2011. PMID: 21093520 Review.
-
Pharmacology of epileptogenesis and related comorbidities in the WAG/Rij rat model of genetic absence epilepsy.J Neurosci Methods. 2018 Dec 1;310:54-62. doi: 10.1016/j.jneumeth.2018.05.020. Epub 2018 May 29. J Neurosci Methods. 2018. PMID: 29857008 Review.
Cited by
-
Tactile stimulation of young WAG/Rij rats prevents development of depression but not absence epilepsy.Front Behav Neurosci. 2024 Jun 27;18:1433431. doi: 10.3389/fnbeh.2024.1433431. eCollection 2024. Front Behav Neurosci. 2024. PMID: 38993266 Free PMC article.
-
The impact of early-life environment on absence epilepsy and neuropsychiatric comorbidities.IBRO Neurosci Rep. 2022 Nov 9;13:436-468. doi: 10.1016/j.ibneur.2022.10.012. eCollection 2022 Dec. IBRO Neurosci Rep. 2022. PMID: 36386598 Free PMC article. Review.
-
Antidepressant and Anxiolytic Effects of L-Methionine in the WAG/Rij Rat Model of Depression Comorbid with Absence Epilepsy.Int J Mol Sci. 2023 Aug 4;24(15):12425. doi: 10.3390/ijms241512425. Int J Mol Sci. 2023. PMID: 37569798 Free PMC article.
-
Maternal Methyl-Enriched Diet Increases DNMT1, HCN1, and TH Gene Expression and Suppresses Absence Seizures and Comorbid Depression in Offspring of WAG/Rij Rats.Diagnostics (Basel). 2023 Jan 21;13(3):398. doi: 10.3390/diagnostics13030398. Diagnostics (Basel). 2023. PMID: 36766503 Free PMC article.
References
REFERENCES
-
- Sarkisova, K. and van Luijtelaar, G., Prog. Neuro-Psychopharm. Biol. Psychiatry, 2011, vol. 35, pp. 854–876.
-
- Sarkisova, K.Yu., Kulikov, M.A., Kudrin, V.S., et al., Zh. Vyssh. Nervn. Deyat. im. I. P. Pavlova, 2014, vol. 63, no. 3, pp. 303–315.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources