Roles of TRPV1 and TRPA1 in Spontaneous Pain from Inflamed Masseter Muscle

Wang, Sheng; Brigoli, Benjamin; Lim, Jongseuk; Karley, Alisha; Chung, Man‐Kyo

doi:10.1016/j.neuroscience.2018.05.048

Cited by 37 publications

(37 citation statements)

References 35 publications

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“…To test effects of focal capsaicin treatment on CCI-induced pain aversion, conditional preference place (CPP) was performed as previously described (Wang et al, 2018). Mice with ION-CCI or sham surgery were conditioned by intra-Vc injection of 2% lidocaine or vehicle with capsaicin or saline pretreatment.…”

Section: Conditioned Place Preference (Cpp) Assaymentioning

confidence: 99%

Ablation of TRPV1+ Afferent Terminals by Capsaicin Mediates Long-Lasting Analgesia for Trigeminal Neuropathic Pain

Wang

Bian

Yang

et al. 2020

eNeuro

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Trigeminal neuropathic pain (TNP) is often resistant to current pharmacotherapy, and there is a pressing need to develop more efficacious treatments. Capsaicin is a pungent ingredient of chili peppers and specifically activates transient receptor potential vanilloid subtype 1 (TRPV1), a Ca 21-permeable ion channel. Topical capsaicin invariably induces burning pain. Paradoxically, the transient pain is often followed by prolonged attenuation of the preexisting pathologic pain from the same region. However, the mechanisms underlying capsaicin-induced analgesia are not well understood. Although the reports of the involvement of TRPV1 and TRPV11 afferents in neuropathic pain are controversial, we recently demonstrated that TRPV1 and TRPV11 afferents are involved in mechanical hyperalgesia in mice with chronic constriction injury of the infraorbital nerve (ION-CCI). Consistently, chemogenetic inhibition of TRPV1-lineage (TRPV1-LN) afferents attenuated mechanical hyperalgesia and ongoing pain. In mice with ION-CCI, we found that a single focal injection of capsaicin into facial skin led to attenuation of mechanical hyperalgesia over two weeks. Capsaicin treatment also attenuated secondary hyperalgesia in extraterritorial mandibular skin. Furthermore, capsaicin treatment decreased ongoing pain. Longitudinal in vivo two-photon imaging of cutaneous nerve fibers showed that such capsaicin-induced analgesia is correlated with cutaneous nerve terminal density. Furthermore, preventing capsaicin-induced ablation of afferent terminals by co-administration of capsaicin with MDL28170, an inhibitor of calpain, abolished capsaicin-induced analgesia. These results suggest that a single focal injection of capsaicin induces long-lasting analgesia for neuropathic pain via selective ablation of TRPV11 afferent terminals and that TRPV11 afferents contribute to the maintenance of TNP.

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Section: Conditioned Place Preference (Cpp) Assaymentioning

confidence: 99%

Ablation of TRPV1+ Afferent Terminals by Capsaicin Mediates Long-Lasting Analgesia for Trigeminal Neuropathic Pain

Wang

Bian

Yang

et al. 2020

eNeuro

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“…The sample size was estimated by power analyses (G*Power version 3.1.9) and previous studies [15,16]. Data are presented as mean (95% confidence interval) for von Frey filament force data (EF 50 ) and mean ± S.E.M.…”

Section: Discussionmentioning

confidence: 99%

“…Several recent studies have employed voluntary bite force to assess complete Freund's adjuvant (CFA)-induced orofacial pain in mice [13][14][15][16]. It appears that a reduction of the bite force occurred mainly within a few days after CFA-induced inflammatory hyperalgesia and the usefulness of the bite force in studying long-lasting pain has not been characterized and evaluated.…”

Section: Introductionmentioning

confidence: 99%

Voluntary biting behavior as a functional measure of orofacial pain in mice

Guo

Zou

Mohammad

et al. 2019

Physiology & Behavior

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Introduction: Pain-related behavior secondary to masticatory function can be assessed with the rodent bite force model. A reduction of the bite force has been shown to be related to pain associated with the masseter muscle and jaw activity, while an increase in bite force suggests improvement of muscle function and less pain. To evaluate the usefulness of the bite force measure in studying long-lasting orofacial pain we analyzed biting parameters during prolonged myofascial pain induced by ligation injury of the masseter muscle tendon (TL) in mice. Methods: C57BI/6 mice were habituated to bite at a pair of aluminum plates attached to a force displacement transducer. The transduced voltage signals were amplified and converted to force through calibration with a standard weight set. Voluntary biting behavior was recorded for 100 seconds/session and those with bite forces ≥ 980 mN were analyzed. Nociception was also verified with von Frey, conditioned place avoidance (CPA) tests and mouse grimace scale. Persistent orofacial pain was induced with unilateral ligation of one tendon of the masseter muscle (TL). Results: To reduce interference of random bites of smaller forces, the top 5 or 15 bite forces (BF5/15) were chosen as a measure of masticatory function and related to pain behavior. Both male and female mice exhibited similar BF5/15. For the first nascent test of all mice, mean bite force was significantly and positively correlated with the body weight. However, this correlation was less clear in the latter tests (2-8 w). TL induced a reduction of BF5/15 that peaked at 1 w and returned to the baseline within 3 w. The von Frey and CPA tests indicated that mechanical

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“…64,65 Simultaneous inhibition of TRPV1 and TRPA1 produces greater conditioned place preference than the respective inhibition, suggesting additive inhibitory effects on ongoing pain. 64 Since masseter inflammation increases the expression of TRPV1 and TRPA1 in TG, 30,63 upregulation of TRPV1 and TRPA1 likely contributes to the hyperalgesia. These results suggest that activation of TRPV1 and TRPA1 mediates spontaneous pain and mechanical hyperalgesia in a rodent model of masseter inflammation.…”

Section: Peripheral Glutamate Induces Craniofacial Muscle Pain and Hymentioning

confidence: 99%

“…In contrast to the inhibitory effects of ablating TRPV1-expressing afferents, the inhibition of TRPV1 molecules only modestly reversed decreased bite force following CFA injection into masseter muscle and the inhibition of TRPA1 did not affect bite force at all. 64,65 Although the source of this discrepancy is unknown, it is hypothesized that unknown molecules expressed in TRPV1-positive masseter afferents mediate bite-evoked nociception under masseter inflammation. Masseter inflammation influences expression of multiple genes from TG implicated in pain processing, 68 and further investigation of their contribution to muscle hyperalgesia, especially in bite-evoked pain, is necessary.…”

Section: Peripheral Glutamate Induces Craniofacial Muscle Pain and Hymentioning

confidence: 99%

Peripheral glutamate receptor and transient receptor potential channel mechanisms of craniofacial muscle pain

Chung

2020

Mol Pain

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Temporomandibular joint disorder is a common chronic craniofacial pain condition, often involving persistent, widespread craniofacial muscle pain. Although the etiology of chronic muscle pain is not well known, sufficient clinical and preclinical information supports a contribution of trigeminal nociceptors to craniofacial muscle pain processing under various experimental and pathological conditions. Here, we review cellular and molecular mechanisms underlying sensitization of muscle nociceptive afferents. In particular, we summarize findings on pronociceptive roles of peripheral glutamate in humans, and we discuss mechanistic contributions of glutamate receptors, including N-methyl-D-aspartate receptors and metabotropic glutamate receptors, which have considerably increased our understanding of peripheral mechanisms of craniofacial muscle pain. Several members of the transient receptor potential (TRP) family, such as transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential ankyrin 1, also play essential roles in the development of spontaneous pain and mechanical hypersensitivity in craniofacial muscles. Furthermore, glutamate receptors and TRP channels functionally and bi-directionally interact to modulate trigeminal nociceptors. Activation of glutamate receptors invokes protein kinase C, which leads to the phosphorylation of TRPV1. Sensitization of TRPV1 by inflammatory mediators and glutamate receptors in combination with endogenous ligands contributes to masseter hyperalgesia. The distinct intracellular signaling pathways through which both receptor systems engage and specific molecular regions of TRPV1 are offered as novel targets for the development of mechanism-based treatment strategies for myogenous craniofacial pain conditions.

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Roles of TRPV1 and TRPA1 in Spontaneous Pain from Inflamed Masseter Muscle

Cited by 37 publications

References 35 publications

Ablation of TRPV1+ Afferent Terminals by Capsaicin Mediates Long-Lasting Analgesia for Trigeminal Neuropathic Pain

Ablation of TRPV1+ Afferent Terminals by Capsaicin Mediates Long-Lasting Analgesia for Trigeminal Neuropathic Pain

Voluntary biting behavior as a functional measure of orofacial pain in mice

Peripheral glutamate receptor and transient receptor potential channel mechanisms of craniofacial muscle pain

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