Thanks for asking!

Millions of people take SSRIs (Selective Serotonin Reuptake Inhibitors) everyday, largely to treat depression, but how do they work, and why is their name so confusing?

Along with some poorly drawn diagrams, this will hopefully explain both.

Figure A. Normal Neurotransmission

In the brain, neurons (nerve cells) communicate through the transmission of electrical signals in a process known as neurotransmission. Neurotransmitters, such as serotonin, dopamine, GABA and others, facilitate this communication. When the pre-synaptic neuron, Neuron A (1), receives an electrical signal (2), it triggers the release of serotonin molecules (4) stored in vesicles (3). These molecules then travel across the gap between neurons, called the synaptic cleft (5). The post-synaptic neuron, Neuron B (7), has specific receptors (6) designed to bind with serotonin molecules. Upon binding, the receptors activate an electrical signal, allowing the communication process to continue into the next neuron (8).

Figure B. Serotonin Reuptake

After the successful transmission of the electrical signal (2), residual serotonin molecules (3) remain in the synaptic cleft (4). Serotonin transporters (1) transport these serotonin molecules back into Neuron A. This allows for the timely termination of the signal, which is important to prevent excessive stimulation of Neuron B. It also allows Neuron A to recover and reuse serotonin for future signalling.

Figure C. SSRIs

The serotonin hypothesis of depression (a hotly contested theory) posits that reduced serotonin activity in the brain plays a significant role in the development of the disorder. Consequently, Selective Serotonin Reuptake Inhibitors (SSRIs, 2) work by binding to serotonin transporters (1) thereby inhibiting their ability to reuptake serotonin. This then increases the concentration of serotonin in the brain.

Figure D. Downregulation of auto-receptors

The increased concentration of serotonin prompts the downregulation (reduction in number or sensitivity) of auto-receptors (2). Auto-receptors (3) signal the neuron to limit further serotonin release in response to elevated concentrations, so as to prevent auto-receptor overstimulation. The outcome of this downregulation is that auto-receptors inhibit serotonin release less, facilitating an increased release of serotonin. The delayed onset of effects (usually 2-4 weeks) when patients start taking SSRIs is attributed to the gradual downregulation of auto-receptors.