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Characterisation of periorbital mechanical allodynia in the reserpine-induced fibromyalgia model in mice: The role of

Evelyne Silva Brum1, Lorenzo Landini2, Daniel Souza Monteiro de Araújo2

  • 1Graduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, 90035-003, Porto Alegre, RS, Brazil; Graduate Program in Biological Sciences: Toxicological Biochemistry, Centre of Natural and Exact Sciences, Federal University of Santa Maria, Santa Maria, RS, Brazil.

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Summary

Fibromyalgia and migraine share links via oxidative stress and TRPA1 channels. Targeting TRPA1 in Schwann cells may treat fibromyalgia-associated headaches.

Keywords:
HeadacheMacrophagesMigraineNADPH oxidaseNociplastic painOxidative stress

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Fibromyalgia (FM) presents with widespread pain and often co-occurs with migraine headaches.
  • Oxidative stress and the TRPA1 channel are implicated in both migraine and FM, but their connection remains unclear.
  • Periorbital mechanical allodynia (PMA) is a key migraine symptom relevant to FM comorbidity.

Purpose of the Study:

  • To investigate the mechanisms linking migraine and FM using a reserpine-induced FM mouse model.
  • To explore the roles of oxidative stress, TRPA1 channels, and macrophages in the trigeminal nerve.
  • To evaluate the therapeutic potential of targeting TRPA1 in Schwann cells for FM-related headaches.

Main Methods:

  • Utilized a reserpine-induced fibromyalgia mouse model.
  • Employed pharmacological interventions, genetic approaches (global deletion, selective silencing), and macrophage depletion.
  • Assessed periorbital mechanical allodynia (PMA), trigeminal nerve neuroinflammation (macrophages, oxidative stress markers).

Main Results:

  • Reserpine induced PMA and trigeminal neuroinflammation, which were ameliorated by antimigraine drugs, macrophage depletion, or TRPA1 inhibition/deletion.
  • Selective TRPA1 silencing in Schwann cells reduced both PMA and neuroinflammation.
  • Selective TRPA1 silencing in sensory neurons reduced PMA but not neuroinflammation.
  • Schwann cell TRPA1 drives oxidative stress and macrophage accumulation, sustaining PMA in FM.

Conclusions:

  • Fibromyalgia-associated headaches involve a feed-forward loop of oxidative stress and neuroinflammation mediated by Schwann cell TRPA1.
  • Targeting TRPA1 channels specifically in Schwann cells presents a promising therapeutic avenue for fibromyalgia and associated headaches.