FoundationalConceptsNeuroscience

the complexities of human behavior, there is often desire to assign
dominant regulatory roles to single molecular entities—in this case,
particular neurotransmitters: oxytocin, the cuddle hormone, love
neuropeptide, compassion molecule; dopamine, the pleasure neuro-
transmitter; and serotonin, the molecular mediator of positive mood.
The serotonin-mood connection derives in large part from the neuro-
chemistry of drugs used to treat what are called mood disorders.
If one becomes stuck for a prolonged period of time (weeks,
months, or more) in a mood state that significantly interferes with
one’s ability to function and flourish in life, one is said to have a mood
disorder. These disorders are generally accompanied by significant
personal suffering. What we call depression (or clinical depression, or
major depression) is a prolonged and dysfunctional dysphoric mood, a
malignant melancholia. A kind of opposite condition is mania, a pro-
longed and dysfunctional euphoric mood—dysfunctional in the sense
that the euphoria is accompanied by poor judgment and grandiosity
that may lead to behaviors that are damaging to oneself and to others.
Manic-depressive disorder (known also as bipolar disorder) is char-
acterized by periods of both mania and depression. In addition, there
are anxiety disorders, characterized by prolonged anxious moods—
chronic, protracted manifestations of nervousness that interfere with
one’s ability to function.
In the 1950s, the first pharmaceutical drugs were serendipitously
discovered that appeared to have specific effects on reducing symp-
toms of depression. By the 1960s there were targeted efforts to
discover more. The first two categories of pharmaceutical antide-
pressants were the monoamine oxidase inhibitors (MAOIs) and the
tricyclic antidepressants (TCAs). Both types of medication appear to
increase the presence of the neurotransmitters norepinephrine and
serotonin at synapses—MAOIs by inhibiting the enzyme (monoamine