Biomarkers of Affective Dysregulation Associated with In Utero Exposure to EtOH DOI Creative Commons
Nune Darbinian, Nana Merabova,

Gabriel Tatevosian

et al.

Cells, Journal Year: 2023, Volume and Issue: 13(1), P. 2 - 2

Published: Dec. 19, 2023

Introduction: Children with fetal alcohol spectrum disorders (FASD) exhibit behavioral and affective dysregulation, including hyperactivity depression. The mechanisms are not known, but they could conceivably be due to postnatal social or environmental factors. However, we postulate that, more likely, the dysregulation is associated effects of EtOH exposure on development serotonergic (5-HT) and/or dopaminergic (DA) pathways, i.e., pathways that in life believed regulate mood. Many women who use (ethanol, EtOH) during pregnancy suffer from depression take selective serotonin reuptake inhibitors (SSRIs), which might influence these monoaminergic fetus. Alternatively, pathway abnormalities reflect a direct effect brain. To distinguish between possibilities, measured their expressions brains brain-derived exosomes (FB-Es) isolated mothers’ blood. We hypothesized maternal SSRIs would impaired neural development, detectable as abnormal levels apoptotic biomarkers FB-Es. Methods: Fetal brain tissues blood were collected at 9–23 weeks pregnancy. groups compared unexposed controls matched for gestational age (GA). expression 84 genes DA 5-HT was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) microarrays. FB-Es also assayed transporter protein (SERT) neurotrophic factor (BDNF) enzyme-linked immunosorbent assay (ELISA). Results: Six EtOH-exposed human samples SSRI- polydrug-exposed controls. significant upregulation receptor D3 HTR2C, while HTR3A downregulated. Monoamine oxidase A (MAOA), MAOB, serine/threonine kinase AKT3, caspase-3 upregulated, mitogen-activated 1 (MAPK1) AKT2 ETOH gene, SERT There correlations (a) activation, (b) reduced levels, (c) BDNF levels. SSRI independently increased activity downregulated BDNF. Early together synergistically downregulation Reduced strongly correlated reduction eye diameter, somatic manifestation FASD. Conclusions: Maternal each changes monoamine consistent potential

Language: Английский

The risks versus the benefits of pharmacological intervention in social anxiety disorder in children DOI Creative Commons
Stefan G. Hofmann, Chantal Kasch, Bruno Pereira

et al.

Expert Review of Neurotherapeutics, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 12

Published: Feb. 12, 2025

Introduction Many children are affected by social anxiety disorder (SAD). Pharmacotherapy, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine (SNRIs), may be indicated, but a clear understanding of the risks benefits associated with these pharmacological treatments is needed.

Language: Английский

Citations

0
Anxiolytic-like action of 3-((4-methoxyphenyl)selanyl)-2-phenylbenzofuran (SeBZF3) in mice: A possible contribution of the serotonergic system DOI

Larissa Sander Magalhães,

Dianer Nornberg Strelow, Mariana Parron Paim

et al.

Pharmacology Biochemistry and Behavior, Journal Year: 2023, Volume and Issue: 232, P. 173651 - 173651

Published: Oct. 2, 2023

Language: Английский

Citations

2
Biomarkers of Affective Dysregulation Associated with In Utero Exposure to EtOH DOI Creative Commons
Nune Darbinian, Nana Merabova,

Gabriel Tatevosian

et al.

Cells, Journal Year: 2023, Volume and Issue: 13(1), P. 2 - 2

Published: Dec. 19, 2023

Introduction: Children with fetal alcohol spectrum disorders (FASD) exhibit behavioral and affective dysregulation, including hyperactivity depression. The mechanisms are not known, but they could conceivably be due to postnatal social or environmental factors. However, we postulate that, more likely, the dysregulation is associated effects of EtOH exposure on development serotonergic (5-HT) and/or dopaminergic (DA) pathways, i.e., pathways that in life believed regulate mood. Many women who use (ethanol, EtOH) during pregnancy suffer from depression take selective serotonin reuptake inhibitors (SSRIs), which might influence these monoaminergic fetus. Alternatively, pathway abnormalities reflect a direct effect brain. To distinguish between possibilities, measured their expressions brains brain-derived exosomes (FB-Es) isolated mothers’ blood. We hypothesized maternal SSRIs would impaired neural development, detectable as abnormal levels apoptotic biomarkers FB-Es. Methods: Fetal brain tissues blood were collected at 9–23 weeks pregnancy. groups compared unexposed controls matched for gestational age (GA). expression 84 genes DA 5-HT was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) microarrays. FB-Es also assayed transporter protein (SERT) neurotrophic factor (BDNF) enzyme-linked immunosorbent assay (ELISA). Results: Six EtOH-exposed human samples SSRI- polydrug-exposed controls. significant upregulation receptor D3 HTR2C, while HTR3A downregulated. Monoamine oxidase A (MAOA), MAOB, serine/threonine kinase AKT3, caspase-3 upregulated, mitogen-activated 1 (MAPK1) AKT2 ETOH gene, SERT There correlations (a) activation, (b) reduced levels, (c) BDNF levels. SSRI independently increased activity downregulated BDNF. Early together synergistically downregulation Reduced strongly correlated reduction eye diameter, somatic manifestation FASD. Conclusions: Maternal each changes monoamine consistent potential

Language: Английский

Citations

2