Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics
in 2 minutes or less.
In this installment I will discuss selective serotonin reuptake inhibitors, or SSRIs.
SSRIs were developed in the 1970s with the goal of treating depression by increasing
serotonin levels.
This goal was formulated based on the serotonin hypothesis of depression, which suggests that
depression is caused by low levels of the neurotransmitter serotonin.
SSRIs work by inhibiting a mechanism called reuptake.
In reuptake, a protein called a transporter transports excess neurotransmitter molecules
out of the synaptic cleft, usually back into the neuron that released them.
SSRIs inhibit the reuptake of serotonin.
By inhibiting the removal of serotonin from the synaptic cleft, this causes levels of
serotonin in the synaptic cleft to rise.
These increases in serotonin levels have been hypothesized to be the mechanism by which
SSRIs can treat the symptoms of depression.
There are reasons now, however, to believe that there must be more to the mechanism of
SSRIs than just changing serotonin levels.
For example, when someone begins taking an SSRI, they generally have to wait about 4
weeks before their symptoms improve.
Evidence suggests, however, that their serotonin levels rise as quickly as within an hour after
taking the medication.
Thus, it seems likely that SSRIs may affect serotonin levels, which then leads to other
effects that influence the symptoms of depression.
Therefore it's probable that more than serotonin levels must be changed for SSRIs to work,
which suggests that depression isn't caused only by low serotonin levels.
Additionally, evidence has now emerged that questions the effectiveness of SSRIs.
Some research has found they do not work much better than placebos, and may only benefit
those who are most severely depressed, which is a minority of patients who actually take
the drugs.
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