FoundationalConceptsNeuroscience

oxidase) that normally inactivates these neurotransmitters by
oxidizing them, and TCAs by blocking or slowing the reuptake of
norepinephrine and serotonin back into the axons of the neurons that
released them. This led to the idea that something to do with increas-
ing the efficacy of norepinephrine and/or serotonin was therapeuti-
cally important for treating the symptoms of depression and that the
mood disorder may even be biochemically precipitated by some kind
of deficit of these neurotransmitters. This came to be called the amine
hypothesis of depression.
For three decades, from the 1950s through the 1980s, the MAOIs
and the TCAs were used to treat clinical depression. While widely
available, they remained essentially a backwater of the pharma-
ceutical industry. Then, in 1988, fluoxetine (Prozac) hit the market,
the first of anew pharmacologic class of antidepressant drugs: the
selective serotonin reuptake inhibitors (SSRIs). Although fluoxetine
and other SSRIs that appeared in the following years—sertraline,
(Zoloft), paroxetine (Paxil), citalopram (Celexa), and so on—were no
more effective than the older MAOIs and TCAs in reducing symptoms
of depression, they had less harmful side effects and were heavily ad-
vertised, quickly becoming best-sellers among pharmaceuticals.
Marketing of these “new-generation” antidepressant medications
was greatly assisted by a loosening during the 1990s of government
restrictions on direct-to-consumer pharmaceutical advertising. Ads
appeared everywhere—in magazines, on billboards, and on television.
Antidepressant medications became big business—very big business.
Because the SSRIs were perceived as nontoxic (at least, it was thought,
relative to MAOIs and TCAs), “nondepressed” people began to use
them to tweak their mood and behavior in the direction of being more
happy, outgoing, and so forth—to become “better than normal,” a
“cosmetic psychopharmacology.”