One of the ways to boost the activity of chemical messengers in the brain is to keep them around longer by preventing them from being taken back into the releasing brain cell (also called a neuron).  This process of chemical messengers, also called neurotransmitters, being shuttled back into the brain cell is termed re-uptake.

There are two main types of antidepressants that work by boosting the activity of mood-enhancing chemical messengers in the brain by blocking reuptake: 1) the SSRIs — Specific Serotonin Reuptake Inhibitors, like Lexapro and Prozac,  and 2) the SNRIs — Serotonin and Norepinephrine Reuptake Inhibitors, like Effexor and Cymbalta. They also work as non-habit-forming treatments for anxiey.  In this post I will explain in more detail how and why reuptake inhibitors work, and in future posts the differences between the SSRIs and SNRIs. One of the theories of depression is that there is deficient activity of  two of the main mood-enhancing neurotransmitters in the brain, serotonin and norepinephrine.

In the emotional centers of the brain, neurons activate each other by releasing these chemical messengers. One neuron will release the neurotransmitter, which travels across a very small space between the neurons and attaches to a docking station, or receptor, on the receiving neuron. If there is enough of this chemical messenger attaching to receptors, then the receiving neuron will be activated, and a signal will have been transmitted (thus the term neuro-transmitter). In depression and anxiety, it is theorized that there is either not enough neurotransmitter being released or that the receptors need more than the typical amount of neurotransmitter to be activated. Because we cannot simply deliver more of these neurotransmitters as a medication, other ways of boosting their activity had to be developed, and one of the main ways is reuptake inhibition.

As above, one of the ways activity of neurotransmitters is regulated is by the releasing neuron bringing the neurotransmitter back into itself after the neurotransmitter has exerted its effect and is floating around in that small gap between the neurons. There is a transporter, or active gait, on the releasing neuron that accomplishes this, by pulling the neurotransmitter back into itself. The reuptake inhibitors, the SSRIS and SNRIs, block that gait, or transporter, preventing the chemical messenger from being taken back into the releasing neuron. This blockade prevents reuptake.

Therefore, there will be more neurotransmitter that stays around in the space between neurons and remains available to activate receptors and boost nerve cell communication and activity. Incidentally, stimulants, like Ritalin, share a similar mechanism of action, but instead are active in blocking dopamine reuptake rather than serotonin or norepinephrine. In treating patients, it is helpful to assess their symptom profile to determine what type of reuptake inhibitor would be best for them.

Regards, Dr. Ranen (Psychiatrist Owings Mills, Baltimore)