FoundationalConceptsNeuroscience

Along with all this came the notion that moods (and perhaps
emotions, too) have some simple relation to brain chemistry—in this
case, serotonin is some kind of happiness molecule, and depression is
related to some kind of deficit in serotonin. The connection between
brain physiology and mood is not likely to be so straightforward,
although it does make for convincing advertising. And certainly sero-
tonergic neurochemistry has something to do with mood—and a lot of
other things, too.
There was a parallel path for antipsychotic medications, drugs
used to reduce disabling delusions and hallucinations in individuals
diagnosed with schizophrenia. Chlorpromazine, the first modern
pharmaceutical antipsychotic, was serendipitously discovered in
the early 1950s in France. It was originally marketed in the United
States as Thorazine. The introduction of chlorpromazine transformed
the practice of psychiatry, and many additional antipsychotic drugs
followed. The first ones were molecular relatives of chlorpromazine;
later, new chemical forms were found. What they all had in common
was antagonist action at dopamine receptors. From this was born the
dopamine hypothesis of psychosis: psychotic symptoms were some-
how related to overactivity in dopaminergic neurotransmission, and
antipsychotic medications reduced the symptoms of psychosis by
blocking some of that overactivity.
Around the time that SSRIs emerged as treatment for depression,
anew generation of antipsychotic medications also came to the
marketplace. These new drugs, like the older antipsychotics, were
dopamine receptor antagonists; in addition, they were antagonists
at certain serotonin receptors and were thus termed serotonin-—
dopamine antagonists. These drugs had side effects that appeared
less problematic than the older antipsychotic medications, providing
a platform for marketing, helped along again by direct-to-consumer