Transient Receptor Potential (TRP) Ion Channels in Orofacial Pain

Luo, Yu‐Hui; Suttle, Abbie; Zhang, Qiaojuan; Wang, Peng; Chen, Yong

doi:10.1007/s12035-021-02284-2

Cited by 29 publications

(22 citation statements)

References 132 publications

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“…In the present study, we found that a membranehyperpolarizing drug retigabine largely prevented the oxaliplatin-induced mechanical and cold hyperalgesia (Du et al, 2014). A previous study also showed that retigabine prevented oxaliplatin-induced orofacial cold hyperalgesia that is likely involved with TRP channels also (Abd-Elsayed et al, 2015;Luo et al, 2021). As retigabine opens potassium channels at resting membrane potential leading to membrane hyperpolarization, these results suggest that targeting oxaliplatininduced membrane depolarization might be a useful strategy to prevent oxaliplatin-induced sensory hyperalgesia.…”

Section: Discussionsupporting

confidence: 79%

Oxaliplatin Depolarizes the IB4– Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice

Zhang

et al. 2021

Front. Mol. Neurosci.

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Use of chemotherapy drug oxaliplatin is associated with painful peripheral neuropathy that is exacerbated by cold. Remodeling of ion channels including TRP channels in dorsal root ganglion (DRG) neurons contribute to the sensory hypersensitivity following oxaliplatin treatment in animal models. However, it has not been studied if TRP channels and membrane depolarization of DRG neurons serve as the initial ionic/membrane drives (such as within an hour) that contribute to the development of oxaliplatin-induced neuropathic pain. In the current study, we studied in mice (1) in vitro acute effects of oxaliplatin on the membrane excitability of IB4+ and IB4– subpopulations of DRG neurons using a perforated patch clamping, (2) the preventative effects of a membrane-hyperpolarizing drug retigabine on oxaliplatin-induced sensory hypersensitivity, and (3) the preventative effects of TRP channel antagonists on the oxaliplatin-induced membrane hyperexcitability and sensory hypersensitivity. We found (1) IB4+ and IB4– subpopulations of small DRG neurons displayed previously undiscovered, substantially different membrane excitability, (2) oxaliplatin selectively depolarized IB4– DRG neurons, (3) pretreatment of retigabine largely prevented oxaliplatin-induced sensory hypersensitivity, (4) antagonists of TRPA1 and TRPM8 channels prevented oxaliplatin-induced membrane depolarization, and (5) the antagonist of TRPM8 largely prevented oxaliplatin-induced sensory hypersensitivity. These results suggest that oxaliplatin depolarizes IB4– neurons through TRPM8 channels to drive the development of neuropathic pain and targeting the initial drives of TRPM8 and/or membrane depolarization may prevent oxaliplatin-induce neuropathic pain.

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Section: Discussionsupporting

confidence: 79%

Oxaliplatin Depolarizes the IB4– Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice

Zhang

et al. 2021

Front. Mol. Neurosci.

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“…Citral, like some other plant compounds, may modulate several different types of TRP ion channels which in the trigeminal system are located in peripheral endings of especially nociceptive afferents, the trigeminal ganglion, and the trigeminal spinal nucleus in the brainstem (Sessle, 2014[ 61 ]; Luo et al, 2021[ 38 ]; Hossain et al, 2019[ 19 ]; Lee et al, 2019[ 33 ]). However, the action of citral is quite complex.…”

Section: Discussionmentioning

confidence: 99%

Transient receptor potential channel involvement in antinociceptive effect of citral in orofacial acute and chronic pain models

Santos

Damasceno

Magalhães

et al. 2022

EXCLI Journal; 21:Doc869; ISSN 1611-2156

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This study aimed to test for the possible antinociceptive effect of the naturally occurring terpene citral in rodent models of acute and chronic orofacial pain and to test for the possible involvement of transient receptor potential (TRP) channels in this effect. Acute nociceptive behavior was induced in one series of experiments by administering formalin, cinnamaldehyde, menthol or capsaicin to the upper lip. Nociceptive behavior was assessed by orofacial rubbing, and the effects of pre-treatment with citral (0.1, 0.3 or 1.0 mg/Kg) or vehicle (control) were tested on the behavior. Nociceptive behavior was also induced by formalin injected into the temporomandibular joint or mustard oil injected into the masseter muscle, preceded by citral or vehicle (control) treatment. The chronic pain model involved infraorbital nerve transection (IONX) that induced mechanical hypersensitivity which was assessed by von Frey hair stimulation of the upper lip. Motor activity was also evaluated. Docking experiments were performed using TRPV1 and TRPM8 channels. Citral but not vehicle produced significant (p<0.01, ANOVA) antinociception on all the acute nociceptive behaviors, and these effects were attenuated by TRPV1 antagonist capsazepine, TRPM3 antagonist mefenamic acid and by TRPM8 desensitization, but not by ruthenium red and TRPA1 antagonist HC-030031. The IONX animals developed facial mechanical hypersensitivity that was significantly reduced by citral but not by vehicle. The docking experiments revealed that citral may interact with TRPV1 and TRPM8 channels. These results indicate the potential use of citral as an inhibitor of orofacial nociception in both acute and chronic pain states through TRPV1, TRPM3 and TRPM8 channels. See also Figure 1 (Fig. 1) .

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“…Moreover, TRPA1 expression is elevated in the odontoblasts of carious teeth 20 . Although the mechanism of dentin hyperalgesia remains unclear, the significant activation of protein expression in many TRP channels in the pulp or DPSCs suggests that TRP channels, specifically TRPA1, have a vital sensory function and play an important role in the pathogenesis of dentin hyperalgesia 28 . TRP channels in DPSCs can be switched on by the corresponding stimuli, thus participating in sensing and responding to various stimuli to ultimately induce hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

TRPA1 triggers hyperalgesia and inflammation after tooth bleaching

Chen

Huang

Zhu

et al. 2021

Sci Rep

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Hyperalgesia has become a major problem restricting the clinical application of tooth bleaching. We hypothesized that transient receptor potential ankyrin 1 (TRPA1), a pain conduction tunnel, plays a role in tooth hyperalgesia and inflammation after bleaching. Dental pulp stem cells were seeded on the dentin side of the disc, which was cut from the premolar buccal tissue, with 15% (90 min) or 40% (3 × 15 min) bleaching gel applied on the enamel side, and treated with or without a TRPA1 inhibitor. The bleaching gel stimulated intracellular reactive oxygen species, Ca2+, ATP, and extracellular ATP in a dose-dependent manner, and increased the mRNA and protein levels of hyperalgesia (TRPA1 and PANX1) and inflammation (TNFα and IL6) factors. This increment was adversely affected by TRPA1 inhibitor. In animal study, the protein levels of TRPA1 (P = 0.0006), PANX1 (P < 0.0001), and proliferation factors [PCNA (P < 0.0001) and Caspase 3 (P = 0.0066)] increased significantly after treated rat incisors with 15% and 40% bleaching gels as detected by immunohistochemistry. These results show that TRPA1 plays a critical role in sensitivity and inflammation after tooth bleaching, providing a solid foundation for further research on reducing the complications of tooth bleaching.

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Transient Receptor Potential (TRP) Ion Channels in Orofacial Pain

Cited by 29 publications

References 132 publications

Oxaliplatin Depolarizes the IB4– Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice

Oxaliplatin Depolarizes the IB4– Dorsal Root Ganglion Neurons to Drive the Development of Neuropathic Pain Through TRPM8 in Mice

Transient receptor potential channel involvement in antinociceptive effect of citral in orofacial acute and chronic pain models

TRPA1 triggers hyperalgesia and inflammation after tooth bleaching

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