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Pathway Description
Fluoxetine Metabolism Pathway
Homo sapiens
Drug Metabolism Pathway
Fluoxetine is a selective serotonin reuptake inhibitor that exerts antidepressive effects by selectively inhibiting serotonin reuptake in the brain. It does so by competing for the same binding site as serotonin on the the sodium-dependent serotonin transporter (SLC6A4). This increases the concentrations of serotonin in the synaptic cleft and reverses the state of low concentration seen in depression. Higher concentration of serotonin has also been shown to have long-term neuromodulatory effects. Binding of serotonin to certain serotonin receptors activate adenylate cyclase, which produces cAMP. cAMP activates protein kinase A which activates cAMP-responsive binding protein 1 (CREB-1). CREB-1 enters the nucleus and affects transcription of brain-derived neurotrophic factor (BDNF). BDNF subsequently stimulates neurogenesis, which may contribute to the long-term reversal of depression.
References
Fluoxetine Pathway References
Prozac. (2009). e-CPS (online version of Compendium of Pharmaceuticals and Specialties). Retrieved December 23, 2009.
Shelton RC: The dual-action hypothesis: does pharmacology matter? J Clin Psychiatry. 2004;65 Suppl 17:5-10.
Pubmed: 15600376
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