The mechanism for SSRIs has been continuously investigated for more than a decade. Explanations of their effectiveness as a class of medications and the lag time associated with their clinical efficacy have implicated the number and sensitivity of SSRI receptor sites, mediated by modulation messages sent from the neuron's nucleus. Is this mechanism still current, or has it been superseded?
The following summarizes at a high level what we know about the importance of the serotonin system in the manifestation of depression, and by extension, its treatment.
“Considerable evidence is now available to support the pivotal role of the serotonin (5-HT) system in exerting the antidepressant response in humans. Different types of antidepressant treatments enhance 5-HT neurotransmission via different pre- or postsynaptic mechanisms. The time course for the occurrence of these adaptive changes in the brain of laboratory animals is consistent with the delayed onset of the antidepressant response in humans.”
Blier, P and de Montigny, C (1998). Possible serotonergic mechanisms underlying the antidepressant and anti-obsessive–compulsive disorder responses. Biological Psychiatry, 44 (5): 313-323.
Given that SSRIs are now by far the most commonly prescribed pharmacological treatment for depression, anxiety, and other conditions impacted by serotonin levels, is there a reason (apart from side effects, perhaps) to treat these psychiatric conditions with anything other than SSRIs. In other words, have we learned anything in recent years that would support an alternative treatment?
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