The vagus nerve is also called the “wandering nerve” because it is the longest nerve in the human body and has countless branches that make their way from the brain stem to the lowest part of the intestines, touching most of the major organs along the way. of the road. The vagus nerve modulates the parasympathetic nervous system, which counteracts the fight-or-flight stress response by eliciting the so-called “relaxation response.”
Every time you exhale, your vagus nerve dumps a little acetylcholine (also known as “vagusstoff”) into your heart. Vagusstoff acts as a tranquilizer-like substance to slow down beat-to-beat intervals and improve heart rate variability (HRV). .
When Prozac was introduced in 1987, it made a huge impact as the first selective serotonin reuptake inhibitor (SSRI) antidepressant for the treatment of major depressive disorder.
Prozac and Sarafem are brand names of a medication called “fluoxetine,” used to treat depression, obsessive-compulsive disorder, panic attacks, and some eating disorders. Historically, most experts and consumers thought that fluoxetine worked by inhibiting the reuptake of serotonin in the brain, and that the antidepressant effects of this medication occurred only from the “neck up.” However, because 90% of serotonin is produced in the gut, one current theory is that fluoxetine may increase the amount of serotonin produced “below the neck.”
While the 21st century debate over SSRIs continues, a non-drug alternative for treatment-resistant depression called “vagus nerve stimulation (VNS)” was approved by the FDA in 2005 for severe unipolar and bipolar depression. VNS usually involves a small silver device that is surgically implanted under the skin near the collarbone and works like a pacemaker to stimulate the vagus nerve.
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In recent years, researchers in Canada have been investigating a possible link between SSRI antidepressant medications, serotonin levels in the gut, and the role that vagus nerve stimulation might play in increasing serotonin transport from the gut to the brain. , which seems to depend on the vagus nerve.
In particular, after a vagotomy, which surgically cuts off the communication through the vagus nerve between the gut and the brain, SSRIs lose their ability to relieve depression symptoms in mice.
As part of the bidirectional gut-brain axis, afferent vagal nerves send signals from the bottom up. There is reason to believe that these vagus nerve pathways could serve as a type of “serotonin superhighway” between the gut and the brain.
The McMaster University team has been conducting research in mice on how SSRIs and the vagus nerve might work together. They published a study that SSRIs can activate the vagus nerve in a way that facilitates serotonin signaling between the gut and the brain (McVey Neufeld et al., 2019).
“The vagus nerve is the tenth cranial nerve and is the main afferent pathway that connects the intestine to the brain. The vagus nerve can transmit signals to the brain, resulting in a reduction in depressive behavior as demonstrated by the long-term beneficial effects of electrical stimulation of the vagus nerve in patients with intractable depression. The vagus is the main neuronal connection between the gut and the brain, and we have previously shown that ingesting beneficial bacteria modulates behavior and brain neurochemistry through this pathway. Given the high levels of serotonin in the gut, we considered whether gut-brain signaling, and specifically the vagal pathway, could contribute to the therapeutic effect of selective serotonin reuptake inhibitors (SSRIs),” the authors explained.
Bibliographic reference:
McVey Neufeld, K.-A., Bienenstock, J., Bharwani, A., Champagne-Jorgensen, K., Mao, Y., West, C., … Forsythe, P. (2019). Oral selective serotonin reuptake inhibitors activate vagus nerve dependent gut-brain signaling. Scientific Reports, 9(1), 14290. https://doi.org/
Fountain: