Intramuscular Temperature Modulates Glutamate-Evoked Masseter Muscle Pain Intensity in Humans

Sato, Hitoshi; Castrillón, Eduardo; Cairns, Brian E.; Bendixen, Karina Haugaard; Wang, Kelun; Nakagawa, Taneaki; Wajima, Koichi; Svensson, Peter

doi:10.11607/ofph.1332

Cited by 7 publications

(5 citation statements)

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“…The results presented in this study suggest that the duration of the glutamate‐evoked pain was longer when it was preceded by a SEMA task. In previous studies, different volumes and concentrations of injections of glutamate (0.1–1 M and 0.2–0.5 ml) into the masseter muscle have been found to evoke about 5–10 min of muscle pain in healthy humans . In the present study, almost all the participants reported pain until the end of the measurement of eVAS (10 min) (Fig.…”

Section: Discussionsupporting

confidence: 63%

Section: Discussionsupporting

confidence: 51%

“…Moreover, it has been reported that injection of 0.5 ml of glutamate (i.e. the same volume as in the present study) did not result in pain lasting longer than 7 min when three different kinds of temperature injection of 0.5 M glutamate were used (51). GAMBAROTA et al suggested that it is the clearance of glutamate that determines the duration of glutamate-evoked pain response and that the clearance of glutamate in the masseter muscle is rapid and appears to be complete in rats 10 min after the injection (53).…”

Section: Discussionmentioning

confidence: 54%

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Influence of glutamate‐evoked pain and sustained elevated muscle activity on blood oxygenation in the human masseter muscle

Suzuki

Arima

Kitagawa

et al. 2017

European J Oral Sciences

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This study aimed to investigate the effect of glutamate-evoked masseter muscle pain on intramuscular oxygenation during rest and sustained elevated muscle activity (SEMA). Seventeen healthy individuals participated in two sessions in which they were injected with glutamate and saline in random order. Each session was divided into three, 10-min periods. During the first (period 1) and the last (period 3) 10-min periods, participants performed five intercalated 1-min bouts of masseter SEMA with 1-min periods of 'rest'. At onset of the second 10-min period, glutamate (0.5 ml, 1 M; Ajinomoto, Tokyo, Japan) or isotonic saline (0.5 ml; 0.9%) was injected into the masseter muscle and the participants kept the muscle relaxed in a resting position for 10 min (period 2). The hemodynamic characteristics of the masseter muscle were recorded simultaneously during the experiment by a laser blood-oxygenation monitor. The results demonstrated that glutamate injections caused significant levels of self-reported pain in the masseter muscle; however, this nociceptive input did not have robust effects on intramuscular oxygenation during rest or SEMA tasks. Interestingly, these findings suggest an uncoupling between acute nociceptive activity and hemodynamic parameters in both resting and low-level active jaw muscles. Further studies are needed to explore the pathophysiological significance of blood-flow changes for persistent jaw-muscle pain conditions.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 54%

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Influence of glutamate‐evoked pain and sustained elevated muscle activity on blood oxygenation in the human masseter muscle

Suzuki

Arima

Kitagawa

et al. 2017

European J Oral Sciences

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“…The analysis failed to find an effect of temperature on masticatory muscle pain reports. In an experimental setting, Sato et al found that injections of hot (48 degrees) isotonic saline into the masseter where not able to determine a significant muscle pain, while hot solutions (48 degrees) of glutamate were able to increase participants pain reports as compared to cold and neutral solutions (29). After the injection, the local temperature increase was about 6 degrees in 10 s. These findings suggest that large and immediate temperature changes within the masseter muscle can affect pain sensitivity.…”

Section: E F F E C T S O F W E a T H E R O N T M D P A I N A N D M I mentioning

confidence: 99%

Effect of weather on temporal pain patterns in patients with temporomandibular disorders and migraine

Cioffi

Farella

Chiodini

et al. 2017

J of Oral Rehabilitation

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Patients with masticatory muscle pain and migraine typically report that the intensity of pain fluctuates over time and is affected by weather changes. Weather variables, such as ambient temperature and humidity, may vary significantly depending on whether the individual is outdoor or indoor. It is, therefore, important to assess these variables at the individual level using portable monitors, during everyday life. This study aimed to determine and compare the temporal patterns of pain in individuals affected with facial and head pain and to investigate its relation with weather changes. Eleven patients (27·3 ± 7·4 years) with chronic masticatory muscle pain (MP) and twenty (33·1 ± 8·7 years) with migraine headache (MH) were asked to report their current pain level on a visual analogue scale (VAS) every hour over fourteen consecutive days. The VAS scores were collected using portable data-loggers, which were also used to record temperature, atmospheric pressure and relative humidity. VAS scores varied markedly over time in both groups. Pain VAS scores fluctuate less in the MP group than in the MH group, but their mean, minimum and maximum values were higher than those of migraine patients (all P < 0·05). Pain scores <2 cm were more common in the MH than in the MP group (P < 0·001). Perceived intensity of pain was negatively associated with atmospheric pressure in the MP group and positively associated with temperature and atmospheric in the MH group. Our results reveal that patients with masticatory muscle pain and patients with migraine present typical temporal pain patterns that are influenced in a different way by weather changes.

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“…69,70 Results in humans are consistent with this mode of interaction between glutamate receptors and TRPV1 signaling: Preceding glutamate administration into masseter causes sensitization to subsequent administration of capsaicin resulting in increasing pain levels and electromyographic activities of the masseter muscle, 71,72 whereas preceding capsaicin administration is associated with a desensitization of nociceptors to subsequent injection of glutamate. 72 Injection of hot or acidic glutamate solution produces greater pain, 73,74 which also suggests heatand acid-mediated regulation of TRPV1. 10 Activation of TRP channels in nociceptors can induce the release of neuropeptides and glutamate from peripheral terminals at the site of injection to produce neurogenic inflammation.…”

Section: Activation Of Trp Channels Leads To Glutamate Receptor Signalingmentioning

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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Intramuscular Temperature Modulates Glutamate-Evoked Masseter Muscle Pain Intensity in Humans

Cited by 7 publications

References 0 publications

Influence of glutamate‐evoked pain and sustained elevated muscle activity on blood oxygenation in the human masseter muscle

Influence of glutamate‐evoked pain and sustained elevated muscle activity on blood oxygenation in the human masseter muscle

Effect of weather on temporal pain patterns in patients with temporomandibular disorders and migraine

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

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