The odontoblast as a sensory receptor cell? The expression of TRPV1 (VR-1) channels

TLDR

Odontoblasts express mechanosensitive channels and may transduce dentinal fluid displacement into neural signals, yet the ionic basis of dentin nociception remains unclear. This study aimed to determine whether rat odontoblasts express the pain‑sensing TRPV1 channel. Immunohistochemistry and nystatin‑perforated patch‑clamp recordings were employed to detect TRPV1 localization and function. TRPV1 immunoreactivity was found on distal odontoblast membranes, and capsaicin‑evoked currents were blocked by capsazepine, indicating that odontoblasts can directly sense noxious stimuli and suggesting a role for TRPV1 in dentin sensation.

Abstract

Previous reports have shown the expression of several mechanosensitive ionic channels on the plasma membrane in odontoblasts, which are the cells responsible for dentin formation. The membrane characteristics of odontoblasts imply that they could play critical roles in the mechano-transduction of fluid displacement within dentinal tubules into the electrical cell signals, to carry dentin sensation to the central nervous system. However, the direct ionic mechanism underlying such a dentin nociceptive function remains unclear. In the present study, we investigated the expression of the transient receptor potential vanilloid subfamily member 1 (TRPV1) channel--which essentially contributes to the detection of pain sensation--in rat odontoblasts by immunohistochemical and nystatin perforated patch-clamp techniques. Immunohistochemical observation showed the localization of TRPV1-immunoreactions on the distal regions of odontoblast membranes. In the patch-clamp experiments, we observed capsaicin-induced inward currents that were inhibited by capsazepine, a TRPV1 channel antagonist. Our results indicate a significant expression of TRPV1 channels in odontoblasts, suggesting that odontoblasts may directly respond to noxious stimuli such as a thermal-heat stimulus, and point to the necessity for a reconsideration of the cellular mechanisms of dentin sensation based on the transmembrane ionic signals in odontoblasts.