The hormone acts as a neurotransmitter which affects the serotonergic neurons in the midline raphe nuclei which are present in the brain stem. The rostral end of this system assists in mood, sleep and vomiting and pain perception. In the case of depression availability of this neurotransmitter is low, though the exact patho-physiology is unknown. Its primary effect is on the muscles and nerves and is stored in enterochromaffin cells of the gut. There it causes the contraction of gastrointestinal smooth muscles dictated by the periphery of the serotonin system. It also promotes platelet aggregation by being stored in them. It also acts as a mediator of inflammation.
Serotonin Syndrome is not caused by the reaction of a single receptor. However, evidence has shown that agonism of the 5-HT2A receptors, such as 5-HT1A may cause the interactions resulting in the increased action of serotonin. Monoamine Oxidase Inhibitors such as those found in Parnate can increase the activity of Serotonin reuptake inhibitors, 5HT1 receptor agonists and most antidepressants leading to a saturation of serotonin activity. The resulting hyper stimulation of the brain stem 5-HT1A and 2A receptors is the cause of Serotonin syndrome. Tranylcypromine and St. John’s Wort is an example of a major drug interaction due to the fact that they are both MAO inhibitors and can cause hyper stimulation of the central nervous system.