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Gene expression in the brain from fluoxetine-injected mouse using DNA microarray
Yasuo Takahashi1, Kazuo Washiyama, Toru Kobayashi
1Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan. yasutakahashi@happytown.ocn.ne.jp
Abstract:
Previously we have examined the effects of phencyclidine and clozapine upon the gene expression in the mouse brain. Recently, fluoxetine (Prozac) has been introduced for the therapeutic purpose as an antidepressant drug. Miledi et al. reported blockage of mouse muscle and neuronal nicotinic acetylcholine receptor by various concentrations of fluoxetine. Furthermore, Kobayashi et al. discovered that fluoxetine inhibits G protein activated inwardly rectifying G protein activated K(+) (GIRK) channels using Xenopus oocyte expression assay. From these experiments, we considered that it might be interesting to study the effects of fluoxetine on the gene expression in the mouse brain. After we have injected fluoxetine once a day into mouse for 20 days, we sacrificed mouse by decapitation and extracted RNA from mouse cerebral cortex. We used DNA microarray method for examining the gene expression in the brain. We found the downregulation of many spot signals in the fluoxetine-treated mouse, for example cholecystockinin and prostaglandin D2 synthase.
Insights
This study investigated fluoxetine
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Fluoxetine (Prozac) is a widely used antidepressant.
- Previous research indicates fluoxetine affects nicotinic acetylcholine receptors and G protein-activated inwardly rectifying potassium (GIRK) channels.
Purpose of the Study:
- To investigate the effects of chronic fluoxetine administration on gene expression in the adult mouse brain.
Main Methods:
- Adult mice were administered fluoxetine daily for 20 days.
- RNA was extracted from the cerebral cortex of treated and control mice.
- DNA microarray analysis was employed to assess genome-wide gene expression changes.
Main Results:
- Fluoxetine treatment led to the downregulation of numerous gene expression signals in the mouse cerebral cortex.
- Specific examples of downregulated genes include cholecystokinin and prostaglandin D2 synthase.
Conclusions:
- Chronic fluoxetine exposure significantly alters gene expression patterns in the mouse brain.
- These findings suggest fluoxetine's antidepressant effects may involve modulation of specific gene pathways, including those related to cholecystokinin and prostaglandin D2 synthase.
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