Malfunctions of the brain's serotonin system are thought to underlie the symptoms of depression, primarily because antidepressants that target the serotonin transporters show some clinical success. We model the experimental data and offer mechanistic insights into how histamine and serotonin modulate one another in health and disease and this leads us to hypothesize why antidepressants are not universally effective. The data afforded by our chemical tools has the capacity to profoundly improve therapeutic strategies towards depression by shedding light on another important player.

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