Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9429850 | Neuroscience Letters | 2005 | 5 Pages |
Abstract
The primary mechanisms of antidepressants are based on the monoamine depletion hypothesis. However, we do not yet know the full cascade of mechanisms responsible for the therapeutic effect of antidepressants. To identify the genes involved in the therapeutic mechanism of the selective serotonin reuptake inhibitor, fluoxetine, we used a cDNA microarray analysis with RBL-2H3 cells. We observed the transcriptional changes of several tens of genes containing the 14-3-3zeta gene in the fluoxetine-treated RBL-2H3 cells. Real-time RT-PCR and Western blotting confirmed changes in the expression of the gene and protein. The increase of 14-3-3zeta mRNA was observed at 72Â h in the fluoxetine-treated RBL-2H3 cells. The increase of 14-3-3zeta protein was observed at 48 and 72Â h. In this study, the expressions of the 14-3-3zeta gene and the protein were up-regulated at 72Â h. In addition, the increase of TPH mRNA was observed at 12, 24 and 72Â h in the fluoxetine-treated RBL-2H3 cells. We conclude that fluoxetine induces increases of 14-3-3zeta mRNA, 14-3-3zeta protein and TPH mRNA at 72Â h in the RBL-2H3 cells. This suggests that the 14-3-3zeta and TPH genes may play a role in the molecular mechanism of fluoxetine. To date, no cases of 14-3-3zeta alterations by antidepressants and specifically by fluoxetine have been reported.
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Neuroscience
Neuroscience (General)
Authors
Seung-Youn Baik, Kyoung Hwa Jung, Mi-Ran Choi, Byung-Hwan Yang, Seok-Hyeon Kim, Jun-Suk Lee, Dong-Yul Oh, Ihn-Geun Choi, Hesson Chung, Young Gyu Chai,