What is the primary action of selective serotonin reuptake inhibitors (SSRIs) like fluoxetine?

Selective serotonin reuptake inhibitors (SSRIs) like fluoxetine primarily function by preventing serotonin from being reabsorbed into the presynaptic neuron. This mechanism allows for an increase in serotonin levels in the synaptic cleft, enhancing serotoninergic neurotransmission. By inhibiting the serotonin transporter (SERT), SSRIs lead to prolonged availability of serotonin to bind to postsynaptic receptors, thereby producing their antidepressant effects.

In contrast, blocking GABA function does not relate to the action of SSRIs, as they specifically target serotonin rather than the inhibitory neurotransmitter GABA. Although some might think increasing serotonin synthesis could contribute to the overall effects of antidepressants, SSRIs do not primarily act by promoting the synthesis of serotonin; instead, they focus on the reuptake process. Additionally, increasing the number of serotonin binding sites is not a direct action of SSRIs; rather, the action of SSRIs is to enhance the existing serotonin's reach and efficacy at its receptors by preventing its reabsorption. This understanding of SSRIs’ mechanism is crucial in pharmacology, particularly in treating mood disorders.