| Abstract: |
| Commonly prescribed selective serotonin reuptake inhibitors (SSRIs) inhibit the serotonin transporter to correct a presumed deficit in extracellular serotonin signaling during depression. These agents bring clinical relief to many who take them; however, a significant and growing number of individuals are resistant to SSRIs. There is increasing evidence that inflammation plays an important role in the clinical variability of SSRIs, though the interactions between SSRIs, inflammation and synaptic serotonin modulation are complex and difficult to discern. This talk will present modeling and data analysis for extracellular serotonin and its co-modulation with inflammation-associated histamine. |
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