PUBLICATION
Risk of prenatal depression and stress treatment: alteration on serotonin system of offspring through exposure to Fluoxetine
- Authors
- Pei, S., Liu, L., Zhong, Z., Wang, H., Lin, S., Shang, J.
- ID
- ZDB-PUB-161007-13
- Date
- 2016
- Source
- Scientific Reports 6: 33822 (Journal)
- Registered Authors
- Lin, Shuo, Wang, Han, Zhong, Zhaomin
- Keywords
- Drug safety, Neurological disorders
- MeSH Terms
-
- Animals
- Depression/drug therapy*
- Depression/metabolism
- Depression/pathology
- Depression/physiopathology
- Fluoxetine/pharmacology*
- Humans
- Induced Pluripotent Stem Cells/metabolism
- Induced Pluripotent Stem Cells/pathology
- Serotonin/metabolism*
- Stress, Psychological/drug therapy*
- Stress, Psychological/metabolism
- Stress, Psychological/pathology
- Stress, Psychological/physiopathology
- Zebrafish/metabolism*
- PubMed
- 27703173 Full text @ Sci. Rep.
Citation
Pei, S., Liu, L., Zhong, Z., Wang, H., Lin, S., Shang, J. (2016) Risk of prenatal depression and stress treatment: alteration on serotonin system of offspring through exposure to Fluoxetine. Scientific Reports. 6:33822.
Abstract
Fluoxetine is widely used to treat depression, including depression in pregnant and postpartum women. Studies suggest that fluoxetine may have adverse effects on offspring, presumably through its action on various serotonin receptors (HTRs). However, definitive evidence and the underlying mechanisms are largely unavailable. As initial steps towards establishing a human cellular and animal model, we analyzed the expression patterns of several HTRs through the differentiation of human induced pluripotent stem (hiPS) cells into neuronal cells, and analyzed expression pattern in zebrafish embryos. Treatment of zebrafish embryos with fluoxetine significantly blocked the expression of multiple HTRs. Furthermore, fluoxetine gave rise to a change in neuropsychology. Embryos treated with fluoxetine continued to exhibit abnormal behavior upto 12 days post fertilization due to changes in HTRs. These findings support a possible long-term risk of serotonin pathway alteration, possibly resulting from the "placental drug transfer".
Errata / Notes
This article is corrected by ZDB-PUB-220906-62.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping