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Antihyperalgesic effect of joint mobilization requires Cav3.2 calcium channels

Daniel F Martins1,2, Victor Sorrentino1, Leidiane Mazzardo-Martins1,2

  • 1Experimental Neuroscience Laboratory (LaNEx), Postgraduate Program in Health Sciences, University of Southern Santa Catarina, Palhoça, SC, Brazil.

Molecular Brain
|July 18, 2023
PubMed

Insights

Joint manipulation (JM) therapy alleviates chronic pain by targeting Cav3.2 T-type channels. This therapy

Area of Science:

  • Neuroscience
  • Pain Research
  • Pharmacology

Background:

  • Peripheral neuropathy and chronic pain are significant challenges.
  • Joint manipulation (JM) therapy shows promise for pain relief.
  • The precise mechanisms underlying JM's analgesic effects require elucidation.

Purpose of the Study:

  • To investigate the role of Cav3.2 T-type channels in mediating the antihyperalgesic effects of JM therapy.
  • To explore potential converging mechanisms involving endocannabinoids.

Main Methods:

  • Utilized the chronic constriction injury (CCI) mouse model to induce peripheral neuropathy.
  • Administered JM therapy to mice with induced chronic pain.
  • Assessed mechanical antihyperalgesia in wild-type and Cav3.2 null mice.
  • Compared JM's analgesic profile with the fatty acid amide hydrolase inhibitor URB597.

Main Results:

  • JM therapy produced long-lasting mechanical antihyperalgesia in mice.
  • The antihyperalgesic effect of JM was completely abolished in Cav3.2 null mice.
  • JM exhibited an analgesic profile similar to URB597, suggesting a role for endocannabinoids.

Conclusions:

  • Cav3.2 T-type channels are essential for the antihyperalgesic activity of JM therapy.
  • JM therapy may act through a mechanism involving endocannabinoids.
  • These findings enhance the understanding of JM's pain-relieving mechanisms.
Keywords:
AnalgesiaCav3.2 channelJoint mobilization therapyMechanical hyperalgesia

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