Drug Deep Dives: SNRIs

The brain is our least understood organ. Research on the structural and functional architecture of the human brain is incredibly...

The brain is our least understood organ. Research on the structural and functional architecture of the human brain is incredibly slow. While it is of the utmost importance that research on the human brain is ethically conducted, you can imagine how difficult it is to study many of the intricacies of the living brain. It is for this reason that new psychiatric treatments are developed at a significantly slower pace than other medical fields. One of the most recent pharmacological innovations in psychiatry came in the early 1990s with the production of the first serotonin AND norepinephrine reuptake inhibitor (SNRI) (Gutierrez, Stimmel, & Aiso, 2003). Today let’s break down the mechanism and function of SNRIs!

As we talked about with SSRIs, reuptake inhibitors block a neuron's ability to vacuum up certain neurotransmitters after they are released. By blocking this, the reuptake inhibitor causes more buildup of free floating neurotransmitters in nervous tissue. This allows the neurotransmitter to activate a neuron for a longer period of time! Like SSRIs, SNRIs increase the level of free-floating serotonin. Unlike SSRIs, SNRIs also increase the level of free-floating norepinephrine (Sansone & Sansone, 2014). So what is norepinephrine? Well, it is a neurotransmitter that helps to regulate emotions, stress responses, and general arousal. A litany of research on this neurotransmitter has shown that it plays a significant role in depression (Briley & Chantal, 2011).

So why take an SSRI versus an SNRI? SSRIs are often the first line of defense against depression, because they have the least amount of side-effects. While SNRIs do not carry a large amount of side-effects, they do carry more than SSRIs (Locher et al, 2017). That said, their general effectiveness in treatment is pretty similar, however SNRIs have shown higher percentages of full remission of depression, compared to SSRIs (Santarsieri & Schwartz, 2015).

The more effective treatments scientists discover, the better our doctors can treat patients with mental illness that is resistant to other treatments. As time presses on, the options for treatment become better and more diverse than before!

Sources:

  • Gutierrez, M. A., Stimmel, G. L., & Aiso, J. Y. (2003). Venlafaxine: A 2003 update. Clinical Therapeutics, 25(8), 2138–2154. https://doi.org/10.1016/s0149-2918(03)80210-2
  • Sansone, R. A., & Sansone, L. A. (2014). Serotonin norepinephrine reuptake inhibitors: a pharmacological comparison. Innovations in Clinical Neuroscience, 11(3-4), 37–42. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008300/
  • Briley, M., & Chantal, M. (2011). The importance of norepinephrine in depression. Neuropsychiatric Disease and Treatment, 9. https://doi.org/10.2147/ndt.s19619
  • Locher, C., Koechlin, H., Zion, S. R., Werner, C., Pine, D. S., Kirsch, I., … Kossowsky, J. (2017). Efficacy and Safety of Selective Serotonin Reuptake Inhibitors, Serotonin-Norepinephrine Reuptake Inhibitors, and Placebo for Common Psychiatric Disorders Among Children and Adolescents. JAMA Psychiatry, 74(10), 1011. https://doi.org/10.1001/jamapsychiatry.2017.2432
  • Santarsieri, D., & Schwartz, T. (2015). Antidepressant efficacy and side-effect burden: a quick guide for clinicians. Drugs in Context, 4, 1–12. https://doi.org/10.7573/dic.212290


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