Search

It is commonly accepted that exposure to stress may cause overactivity in the orofacial muscles, leading to consistent muscle pain, which is the main symptom of temporomandibular disorders. The central neural mechanism underlying this process, however, remains unclear. The locus coeruleus is considered to play an important role in stress-related behavioral changes. Therefore, the present study was designed to examine the role of locus coeruleus neurons in masseter overactivity induced by stress. C57BL/6 mice were subjected to chronic restraint stress for 14 days to establish an animal model. The behavioral changes and the electromyography of the masseter muscle in mice were measured. The expression of Fos in locus coeruleus was observed by immunofluorescence staining to assess neuronal activation. A chemogenetic test was used to inhibit locus coeruleus neuronal activity, and the behavioral changes and electromyography of the masseter muscle were observed again. The results exhibited that chronic restraint stress could induce anxiety-like behavior, overactivity of the masseter muscle, and significant activation of locus coeruleus neurons in mice. Furthermore, inhibition of noradrenergic neuron activity within the locus coeruleus could alleviate stress-induced anxiety behavior and masseter muscle overactivity. Activation of noradrenergic neurons in locus coeruleus induced by stress may be one of the central regulatory mechanisms for stress-induced anxiety-like behaviors and overactivity of masseter muscles., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

It is commonly accepted that psychological stress contributes to the development of chronic orofacial pain. However, the neural mechanism underlying this process has remained unclear. The present study was performed to determine the involvement of satellite glia cells (SGCs) in the trigeminal ganglion (TG) in stress-induced increases in masseter muscle allodynia in rats. Using a chronic restraint stress model, we found that exposure to a 14-day stress but not a 3-day stress (6 h/day) caused decreased body weight gain, behavioral changes and marked masseter allodynia in rats. SGCs were dramatically activated, and substance P (SP) expression was significantly increased in the TG. A further analysis was undertaken to investigate the contribution of SGCs; the expression of interleukin-1β (IL-1β) in SGCs and interleukin-1 receptor I (IL-1RI) in neurons was significantly increased after chronic restraint stress, whereas injection of L-α-aminoadipate (a SGC inhibitor, LAA) into the TG dramatically inhibited the overexpression of these proteins. In addition, LAA or interleukin-1 receptor antagonist (IL-1ra) administration into the TG could significantly attenuate the mechanical masseter allodynia and overexpression of SP in the TG induced by restraint stress. These results suggest that SGC activation in the TG may play a role in masseter allodynia induced by restraint stress. The over-release of IL-1β and excessive IL1-RI expressions have close relationship with the stress induced masseter allodynia., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

It is commonly accepted that psychological stress contributes to the development of temporomandibular joint disorders, in which chronic orofacial pain is the main symptom. However, the central mechanism underlying the development of these disorders has remained unclear. The current study was performed to determine the involvement of the glia in the trigeminal spinal subnucleus caudalis in stress-induced increases in masseter muscle hyperalgesia in rats. After being subjected to chronic restraint stress, the animals showed decreased body weight gain, behavioral changes and marked masseter allodynia. We also found that astrocytes, but not microglia, in the trigeminal subnucleus caudalis (Vc) were dramatically activated. A further analysis was undertaken to investigate the contribution of the glia; we intrathecally injected l-α-aminoadipate (astrocyte-specific inhibitor) and/or minocycline (microglia-specific inhibitor) into the stressed rats. Our results showed that l-α-aminoadipate (LAA), but not minocycline, could significantly attenuate the mechanical masseter allodynia and behavioral changes induced by restraint stress. In addition, the expression of interleukin-1β (IL-1β) and phosphorylated N-methyl-d-aspartic acid receptor 1 (p-NR1) in the Vc was significantly increased after chronic restraint stress, whereas LAA dramatically inhibited the overexpression of IL-1β and p-NR1. Taken together, these results suggest that activated astrocytes in the Vc may be one of the most important factors in the pathophysiology of masseter hyperalgesia induced by restraint stress and the following overexpression of IL-1β and excessive NMDAR phosphorylation may ultimately contribute to masseter hyperalgesia. Thus, inhibiting spinal astrocytic activation may represent a novel therapeutic strategy for the treatment of orofacial pain induced by stress., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Experimental and non-experimental stress significantly increase masseter muscle tone, which has been linked to the symptoms and pathogenesis of several stomatognathic system diseases. Until now, the mechanism underlying this phenomenon has remained unclear. The current study was performed to determine the mechanism of the stress-induced increase in masseter muscle tone and to investigate the effect of lamotrigine on this change. Animals challenged by repeated restraint stress received either saline as a vehicle or lamotrigine in doses of 20, 30 or 40 mg/kg body weight, whereas control animals received saline without stress treatment. Masseter muscle tone was assessed using electromyography. The activity of glutamate-related metabolic enzymes (glutaminase and glutamine synthetase) in the trigeminal motor nucleus was also investigated. Our results showed an interesting phenomenon: masseter muscle activity increased concurrently with the upregulation of the glutamate concentration after stress treatment. The activities of glutaminase and glutamine synthetase in the trigeminal motor nucleus were also upregulated and downregulated, respectively, when the rats were challenged by prolonged stress. The animals treated with lamotrigine at moderate and high doses had significantly decreased masseter muscle tone compared with stressed animals treated with vehicle. These results suggested that increased glutaminase activity and decreased glutamine synthetase activity increased glutamate production and decreased glutamate decomposition, causing an increase in glutamate levels in the trigeminal motor nucleus and eventually increasing masseter muscle tone. The administration of lamotrigine at doses of 30 or 40 mg/kg body weight effectively mitigated the adverse effects of stress on masseter muscle tone via inhibition of glutamate release., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Objective: To investigate the correlation between psychological stress and masseter muscle (MM) alterations, and explore the therapeutic agents for restoring the impaired masticatory muscle., Design: We established a chronic unpredictable mild stress (CUMS) animal model and observed the changes of ultrastructure, redox homeostasis and energy metabolism in MM in rats with and without curcumin treatment., Results: The depressive-like behavior in stressed rats was confirmed by the evidences of altered behaviors in sucrose preference test and open field test; while these phenomena were eased by curcumin. Except for the pathological changes in ultrastructure, decreased SOD, GSH-Px, CAT, Na(+)-K(+)ATPase, and Ca(2+)-Mg(2+)ATPase activities as well as increased MDA and LD content and LDH activity were also observed in MM in stressed rats. However, curcumin was capable of reversing CUMS-induced MM disorder by improving the activities of the examined anti-oxidant enzymes and energy metabolism enzymes. Additionally, the increased MDA content, LD content, and LDH activity in stressed rats were reduced by curcumin., Conclusion: All the findings indicate the adverse effects of CUMS on MM function in rats, and raise the possibility of developing curcumin as a potential therapeutic agent for psychological stress-induced masseter dysfunction., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Psychological stressors are generally associated with masseter muscle dysfunction and disorders in emotional response. In addition, oxidative states and HSP70 expression, which are involved in the physical and pathological changes of the masseter muscle, could be altered in the stressed tissues and organs. However, the link between psychological stress and the redox homeostasis or the expression of HSP70 in masseter muscles in rats has not been examined. Therefore, we used a communication box paradigm to induce psychological stress in rats. The successful establishment of the animal model was evidenced by an increase in plasma corticosterone and adrenocorticotropic hormone (ACTH). Meanwhile, the stressed rats showed a decrease in the number of entries on open arms, percentage of time spent in open arms, and distance moved in the elevated plus-maze test. The stressed rats also displayed a decrease in the time spent in the center zone, active velocity, and the distance moved in the open-field test. These results demonstrate affective-like behavioral changes in the stressed rats. Moreover, compared with the control rats, a decrease in SOD, GSH-Px and catalase activities and an increase in MDA content were observed in the masseter muscles in stressed rats after 3 weeks and 5 weeks, and the HSP70 expression was elevated in muscles in the rats exposed to stress for 5 weeks. These results indicate that psychological stress induces oxidative damage and up-regulates the expression of HSP70 in masseter muscles in rats, which are associated with behavior resembling anxiety., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objective: To study the influence of emotion stress on mechanical hyperalgesia of masseter muscles in rats through the equipment of communication box., Methods: 50 Sprague-Dawley rats were randomly divided into 5 groups: Control group, emotion stress (ES) group, drug control group, saline treated control group and footshock (FS) group, 10 rats each group. Footshock group only induced emotion stress and was not concerned with the result of the experiment. The last four groups of the rats were placed in communication box and bred under the same conditions during the experiment time. According to Rens' method, von Frey filaments were used to assess the muscle mechanical threshold, head withdrawal, leg raising and crying were observed as pain action., Results: 1) During the adaptive period of 7 days before the emotion stress experiment, mechanical pain values of bilateral masseter muscles were descent and were stabilized in the 5 th to 7 th day. In emotion stress period, hyperalgesia of emotion stress group was induced in bilateral masseter muscles, and the peak time was the 7 th day, then it alleviated in the following days and was stabilized in the 12 th to 14 th day, but its pain threshold was lower than blank control group. 2)During the emotion stress period, the change of drug control group was similar to stress group but its pain threshold was higher., Conclusion: It is suggested that emotion stress can lead to the hyperalgesia of masseter muscles and antidepressant drug can lower the hyperalgsia resulted of emotion stress.

Psychological stress is commonly accepted to be closely associated with masticatory muscle disorder, which is the main symptom of temporomandibular disorder (TMD). Previous studies have confirmed that exposure to stress may cause masticatory muscle hyperactivity. However, the central mechanism underlying this process remains unclear. The mesencephalic trigeminal nucleus (Vme), which resides in the brainstem, is the primary afferent center for masticatory proprioception and plays a key role in oral–motor movements by projecting to the trigeminal motor nucleus (Vmo). Therefore, the present study was designed to examine the role of Vme neurons in masseter overactivity induced by chronic stress. We found that subjecting mice to restraint stress (6 h/day) for 14 days caused significant anxiety-like behavior, obvious masseter overactivity, and markedly enhanced electrophysiological excitability of Vme neurons. By using anterograde tract tracing combined with immunofluorescence staining methods, we observed vesicular glutamate transporter 1 (VGLUT1)-positive glutamatergic projections from the Vme to the Vmo. Moreover, chronic restraint stress (CRS) elevated the expression of VGLUT1 and choline acetyltransferase (ChAT) in Vmo. Furthermore, administration of VGLUT1-targeted short hairpin RNA (shRNA) into the bilateral Vme significantly suppressed the enhanced overexcitability of Vme neurons, downregulated the overexpression of VGLUT1 and ChAT in the Vmo, and attenuated the elevated overactivity of the masseter caused by CRS. Taken together, we showed that CRS can excite neurons in the Vme, enhancing glutamatergic excitatory projections from the Vme to the Vmo and resulting in masseter muscle overactivity. These findings provide us with a novel central mechanism underlying the correlation between psychological factors and TMD. [ABSTRACT FROM AUTHOR]

Background and objective: Psychological stress causes structural and metabolic dysfunction of masseter muscles. The anti‐inflammatory and anti‐oxidative polyphenol curcumin plays a local antioxidant role in rat masseter muscles under psychological stress by an as‐yet‐unknown mechanism. The present study aimed to assess curcumin anti‐inflammatory and anti‐oxidative effects on masseter muscle and its possible molecular mechanisms. Methods: We constructed a rat model of chronic unpredictable moderate stress (CUMS). Psychological stress was assessed by determining the levels of adrenocorticotropic hormone (ACTH) and cortisol in serum. Enzyme‐linked immunosorbent assays measured inflammatory cytokines and markers of oxidative stress in masseter muscles. Levels of high‐mobility group box 1 (HMGB1), interleukin (IL)‐1β, IL‐6 and tumour necrosis factor‐alpha (TNF‐α) were determined using quantitative PCR analyses and immunofluorescent staining. Toll‐like receptor 4 (TLR4) and nuclear factor kappa B (NF‐κB) activation were examined using western blotting. Results: The CUMS group showed increased serum cortisol and ACTH levels. Pathological changes in the ultrastructure, oxidative stress and inflammatory cytokines in the masseter muscles were also observed. Curcumin treatment (50, 100 mg/kg) ameliorated these changes significantly by varying degrees. Mechanistically, increased levels of phosphorylated NF‐κB, toll‐like receptor 4 and HMGB1 were observed, which were also ameliorated by curcumin treatment. Conclusion: Curcumin can reduce local pathological changes, levels of oxidative stress and inflammatory factors in masseter muscles. Psychological stress activates HMGB1 expression and increases the expression of downstream TLR4 and p‐NF‐κB, which could be reduced by curcumin. Thus, curcumin might exert anti‐inflammatory and antioxidant effects in masseter muscles via the HMGB1/TLR4/NF‐κB pathway. [ABSTRACT FROM AUTHOR]