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Serotonin-norepinephrine reuptake inhibitors, or SNRIs, first appeared on the market in
1993 with the introduction of venlafaxine.
Several others, like duloxetine, would be introduced in the following decades.
Most SNRIs were primarily developed for the treatment of depression, but some are now
also used to treat a variety of other conditions like anxiety and chronic pain.
The development of SNRIs was guided by research that suggests neurotransmitters like serotonin
and norepinephrine play a role in depression.
Specifically, this research suggests that low levels of these neurotransmitters might
contribute to the symptoms of depression.
SNRIs work primarily by inhibiting a mechanism called reuptake.
In reuptake, a protein called a transporter transports excess neurotransmitter molecules
out of the synaptic cleft, and typically back into the neuron that released them.
SNRIs inhibit the reuptake of serotonin and norepinephrine.
When the removal of serotonin and norepinephrine from the synaptic cleft is inhibited, this
causes levels of these neurotransmitters in the synaptic cleft to rise.
These increases in serotonin and norepinephrine levels have been hypothesized to be the mechanism
by which SNRIs can treat the symptoms of depression.
It should be noted, however, that research suggests the neurobiological mechanism of
depression is more complex than a simple neurotransmitter deficiency.
Thus, it may be that increasing serotonin and norepinephrine levels leads to other effects
that can alleviate the symptoms of depression, or that the drugs have other mechanisms that
contribute to their effectiveness.
Studies have found SNRIs to be comparable to other popular antidepressants, like SSRIs,
in terms of effectiveness.
SNRIS are also generally well-tolerated, with problems like nausea, sweating, and loss of
appetite being some of the commonly reported side effects---although different snri drugs
have different side effect profiles.