Electroacupuncture Mitigates TRPV1 Overexpression in the Central Nervous System Associated with Fibromyalgia in Mice.

Fibromyalgia causes widespread chronic pain along with fatigue, sleep problems, and other symptoms that significantly impact daily life. Researchers investigated whether electroacupuncture could help relieve fibromyalgia pain by affecting a specific pain receptor called TRPV1 in the brain and spinal cord. Scientists created a fibromyalgia-like condition in mice using intermittent cold stress, which caused the animals to develop increased sensitivity to touch and temperature. They then treated some mice with electroacupuncture at the ST36 acupoint (located on the lower leg) using a 2 Hz frequency, while comparing results to untreated mice, mice receiving fake acupuncture, and mice genetically modified to lack the TRPV1 receptor. The study found that electroacupuncture significantly reduced both mechanical and thermal pain sensitivity over a 21-day period. Mice receiving real electroacupuncture showed improvements similar to those lacking the TRPV1 receptor entirely, while fake acupuncture produced no benefits. Laboratory analysis revealed that fibromyalgia increased TRPV1 and pain-related proteins throughout multiple brain regions, including the thalamus, cortex, hippocampus, and cerebellum. Electroacupuncture successfully reduced this overexpression of pain proteins. These findings suggest that electroacupuncture may help fibromyalgia patients by modulating TRPV1 activity in the central nervous system, offering a potential treatment option for managing chronic widespread pain. Patients interested in acupuncture for fibromyalgia should seek treatment from a licensed acupuncturist trained in electroacupuncture techniques.

This preclinical study examined electroacupuncture's effects on TRPV1-mediated central sensitization in a murine fibromyalgia model induced by intermittent cold stress (ICS). Five groups were evaluated (n=6): control, ICS, ICS+EA, ICS+sham EA, and ICS+TRPV1 knockout. Mechanical withdrawal thresholds improved from 2.43±0.19g (day 14) to 5.88±0.47g (day 21) with 2 Hz EA at ST36, while thermal latency increased from 2.77±0.22s to 5.85±0.41s (p<0.05). Western blot analysis demonstrated significant TRPV1 and pain-related protein upregulation across multiple CNS regions (thalamus, somatosensory cortex, mPFC, hippocampus, hypothalamus, cerebellar regions V-VII) in the ICS model. Both EA and TRPV1 knockout significantly attenuated this protein overexpression; sham EA showed no effect. Clinical implications suggest EA at ST36 may modulate central TRPV1 pathways in fibromyalgia management, with effects comparable to TRPV1 antagonism, supporting its use for chronic widespread pain.