Тип публикации: статья из журнала

Год издания: 2017

Идентификатор DOI: 10.1016/j.neulet.2017.05.070

Ключевые слова: C1473G polymorphism, Congenic mice, Fluoxetine, Serotonin, Tryptophan hydroxylase 25 hydroxyindoleacetic acid, 1321-73-9, 54-16-0, DNA directed RNA polymerase, fluoxetine, 54910-89-3, 56296-78-7, 59333-67-4, serotonin, 50-67-9

Аннотация: Selective serotonin reuptake inhibitors (SSRIs) are antidepressants that block serotonin transporter (SERT) and increase serotonin (5-HT) level in the synaptic cleft. The interaction between SERT and the key enzyme of 5-HT synthesis in the brain, tryptophan hydroxylase 2 (TPH2), is essential to maintain the brain 5-HT level. The G Показать полностьюallele of C1473G polymorphism in Tph2 gene decreases enzyme activity by half in mouse brain. Here we studied effect of C1473G polymorphism on the reaction of brain 5-HT system to chronic fluoxetine treatment (120 mg/l in drinking water, for 3 weeks) in adult males of the congenic B6-1473C and B6-1473G mouse lines with high and low enzyme activity, respectively. The polymorphism did not affect the levels of 5-HT, its metabolite, 5-hydroxyindoleacetic acid (5-HIAA) and Tph2 gene mRNA in the brain. Fluoxetine significantly attenuated 5-HT levels in the cortex and striatum, 5-HIAA concentrations in the cortex, hippocampus, striatum and midbrain, and Tph2 gene expression in the midbrain. However, we did not observed any effect of the genotype x treatment interaction on these neurochemical characteristics. Therefore, C1473G polymorphism does not seem to play an essential role in the reaction of the brain 5-HT system to chronic fluoxetine treatment. © 2017 Elsevier B.V.

Журнал: Neuroscience Letters

Выпуск журнала: Vol. 653

Номера страниц: 264-268

ISSN журнала: 03043940

Издатель: Elsevier Ireland Ltd

• Bazhenova E.Y. (Department of Genetic Models of Neuropathologies, Federal Research Center Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Science, Novosibirsk, Russian Federation)
• Sinyakova N.A. (Department of Genetic Models of Neuropathologies, Federal Research Center Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Science, Novosibirsk, Russian Federation)
• Kulikova E.A. (Laboratory of Behavioral Neurogenomics, Federal Research Center Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Science, Novosibirsk, Russian Federation)
• Kazarinova I.A. (Novosibirsk State University, Novosibirsk, Russian Federation)
• Bazovkina D.V. (Laboratory of Behavioral Neurogenomics, Federal Research Center Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Science, Novosibirsk, Russian Federation)
• Gainetdinov R.R. (Institute of Translational Biomedicine, St. State University, Petersburg, Russian Federation, Skolkovo Institute of Science and Technology, Skolkovo, Moscow, Russian Federation)
• Kulikov A.V. (Department of Genetic Models of Neuropathologies, Federal Research Center Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Science, Novosibirsk, Russian Federation)

• Scopus