Why Inflammation Boosts Vagus Nerve Signaling By 2.3 Fold
Your Vagus Nerve *loves* inflammation, so much it boost Vagal signaling 2.3 fold !
This might be why people who are using VNS (Ultrasound, electrical, etc) - may actually only need to use a little bit, since their Vagus Nerve is going to activate more, with less, very interesting study !
The vagus nerve is traditionally categorized as the primary conduit for "rest and digest" functions. However, recent research on acute pancreatitis reveals it also serves as a critical, inflammation-triggered pain superhighway.
In mice, caerulein-induced inflammation upregulates nociceptive markers such as TRPV1, Nav1.8, and CGRP within subdiaphragmatic vagal afferents. This enables the vagus to co-transmit visceral pain signals alongside traditional spinal pathways.
Using NaV1.8-Cre mice and chemogenetic inhibition (hM4Di-DREADD), studies show that silencing these vagal fibers reduces pain behaviors by up to 62%. Inflammation increases vagal neuron excitability 2.3-fold, projecting directly to the nucleus tractus solitarius (NTS).
These findings position the vagus nerve as a high-precision target for neuromodulation. Vagus Nerve Stimulation (VNS) could eventually provide a non-opioid alternative for managing the intense agony associated with pancreatic inflammation.
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Sterling Cooley
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Why Inflammation Boosts Vagus Nerve Signaling By 2.3 Fold
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