Blocking the recycling pump
An SSRI — selective serotonin reuptake inhibitor — does exactly what the name says. After serotonin is released into the gap, a transporter called the serotonin transporter normally pumps it back into the neuron. An SSRI blocks that pump. Serotonin builds up in the gap and keeps signalling. As reuptake inhibitors, SSRIs raise serotonin's signal selectively, leaving other systems largely alone — which is why they cause fewer side effects than older antidepressants.
Starting, adjusting, and stopping
- Start low. Beginning at a small dose limits early nausea, jitteriness, and sleep changes that can otherwise scare a patient off.
- Wait. Because the benefit is delayed, give an adequate dose several weeks before judging it a failure — this is the heart of dose titration for depression.
- Adjust or switch. If there is no response at a proper dose and duration, titrate up or change agent rather than abandoning treatment.
- Taper to stop. Stopping abruptly can cause discontinuation symptoms (dizziness, electric-shock sensations, mood dips), so reduce gradually.
The main indication is depression, but SSRIs also treat anxiety disorders, panic, and obsessive-compulsive disorder. Their most feared adverse reaction is serotonin syndrome — too much serotonin all at once, with agitation, fever, tremor, and racing heart. It is rare on an SSRI alone but a real drug interaction danger when combined with other serotonin-raising drugs.
Older and other antidepressants
Before SSRIs came the monoamine oxidase inhibitors, which block the enzyme that breaks serotonin, norepinephrine, and dopamine down inside the neuron. They work, but combined with certain foods (aged cheese, cured meats) they can cause a dangerous blood-pressure spike — which is why they are now reserved cases. Some newer antidepressants deliberately raise both serotonin and norepinephrine, on the idea that two messengers may help where one is not enough.