What is the mechanism of action of selective serotonin reuptake inhibitors (SSRIs)?

Selective serotonin reuptake inhibitors (SSRIs) function primarily by blocking the reuptake of serotonin into presynaptic neurons. This mechanism enhances the availability of serotonin in the synaptic cleft, which increases serotonergic neurotransmission. When SSRIs inhibit the serotonin transporter (SERT), it prevents the reabsorption of serotonin that has been released into the synaptic cleft back into the presynaptic cell, thereby prolonging the action of serotonin on the postsynaptic receptors. This is a key factor in the treatment of depression and anxiety disorders, as it raises the overall serotonin levels that influence mood and emotional regulation.

The other choices describe mechanisms that do not align with the primary action of SSRIs. For example, increasing dopamine levels or enhancing norepinephrine release are not actions associated with SSRIs; instead, they are more relevant to other classes of medications such as dopaminergic agents or norepinephrine reuptake inhibitors. Reducing serotonin synthesis would counteract the therapeutic effects of SSRIs, as the goal is to increase serotonin availability rather than decrease it. Therefore, the correct understanding of the mechanism of SSRIs centers on their ability to inhibit serotonin reuptake, which is vital for their antidepressant action.