Role of trigeminal ganglion satellite glial cells in masseter muscle pain hypersensitivity

Abstract

Objectives: The underlying mechanism of masseter muscle pain hypersensitivity by sustained masseter muscle contraction (SMMC) is not well understood. This study aimed to examine whether the activation of satellite glial cells in the trigeminal ganglion (TG) contributes to masseter muscle pain hypersensitivity induced by SMMC.

Methods: Electrodes were placed on the masseter muscle fascia of rats to induce strong contractions, by daily electrical stimulation. Pain sensitivity in the masseter muscle was measured and the activation level of satellite glial cells in the TG was examined. The localization of P2Y₁₂ and the effects of P2Y₁₂ receptor inhibition on SMMC-induced pain hypersensitivity were evaluated. The amount of tumor necrosis factor alpha (TNF-α) and TNF-α receptor localization were determined in the TG.

Results: SMMC induced masseter muscle pain hypersensitivity and activation of satellite glial cells. P2Y₁₂ receptors were expressed in satellite glial cells and masseter muscle pain hypersensitivity was suppressed by intra-TG P2Y₁₂ receptor antagonism. TG neurons innervating the sustained-contracted masseter muscle expressed TNF-α receptor and SMMC increased TNF-α levels in TG.

Conclusion: SMMC-induced activation of satellite glial cells though the P2Y₁₂ receptor signaling may contribute to masseter muscle pain hypersensitivity via the TNF-α signaling pathway.

Keywords: Masseter muscle contraction; Mechanical allodynia; P2Y(12); Satellite glial cell; Tumor necrosis factor alpha.