Recent advances in basic research on the trigeminal ganglion

Goto, Tetsuya; Oh, Seog Bae; Takeda, Masatoshi; Shinoda, Masamichi; Sato, Tadasu; Gunjikake, Kaori K.; Iwata, Koichi

doi:10.1007/s12576-016-0448-1

Cited by 36 publications

(33 citation statements)

References 28 publications

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“…23, 25 Alternatively, frequent low intensity muscle activity may be a sign of homeostatic dysregulation. This has been demonstrated recently by data from animal models showing that increased activity of the sympathetic nervous system resulted in increased trigeminal motor neuron excitability 26 and glial cell-mediated neuroplasticity of trigeminal ganglia primary afferents 27 and subnucleus caudalis interneurons, 28 and showing associations between stress, autonomic nervous system (ANS) dysregulation, and masticatory muscle activity. 29 In humans, increased masticatory muscle activities at low levels during sleep in subjects with self-reported anxiety and somatization compared to control subjects have been reported.…”

Section: Discussionmentioning

confidence: 84%

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

Wei

Horn

Coombs

et al. 2017

J of Oral Rehabilitation

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Background Temporomandibular disorder (TMD) incidences are believed to be related to parafunctional behaviors like teeth clenching. Objectives This pilot study aimed to (i) develop an automated clench-detection algorithm, and (ii) apply the algorithm to test for differences in nocturnal clenching in women with and without TMD. Methods Subjects gave informed consent to participate. Adult women were categorized using Diagnostic Criteria for TMD according to presence/absence (+/-) of both TM joint disc placement (DD) and chronic pain (P) into two groups (+DD+P, -DD-P) with 12 subjects each. Surface temporalis electromyography was recorded during oral tasks performed by subjects at two laboratory sessions. The data were used to characterize muscle activity per N of bite-force (μV/N) for each subject, develop the clench-detection algorithm and test its accuracy. Ambulatory surface temporalis electromyography was self-recorded by each subject over three nights and analyzed using the algorithm and bite-force (N) vs muscle activity μV/N calibrations. Bonferroni-adjusted homoscedastic t-tests assessed for significant between-group differences in clenching (p<0.05). Results Sensitivity, specificity, and accuracy of algorithm-detected laboratory clenches were all ≥96%. During self-recordings 95% of clenches had durations of <4 seconds and peak forces of <10 N in both groups. Mean clench durations were significantly longer (p=0.042) in +DD+P (1.9±0.8 seconds) than -DD-P subjects (1.4±0.4 seconds). Mean temporalis duty factors (%clench time/total recording time) were significantly larger (p=0.041) in +DD+P (0.47±0.34%) than -DD-P (0.26±0.22%) subjects. Conclusions Nocturnal temporalis muscle activities detected by a validated algorithm were longer per clench and recording time in +DD+P compared to -DD-P women.

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Section: Discussionmentioning

confidence: 84%

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

Wei

Horn

Coombs

et al. 2017

J of Oral Rehabilitation

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“…Experimental evidence suggests that satellite glial cells in the TG release a variety of molecules that modulate TG neuron excitability under normal circumstances and increase excitability when they are persistently activated by noxious stimuli [174]. However, the role that satellite glial cells play in modifying the excitability of TG neurons that supply the ocular surface has not yet been investigated.…”

Section: Neurobiological Features In Normal/non Dry Eye Diseasementioning

confidence: 99%

TFOS DEWS II pain and sensation report

et al. 2017

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Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglia mechano- and polymodal nociceptor neurons while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of Meibonian gland secretion or mucins release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.

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“…29,30 However, its role in inflammatory pain remains poorly elucidated. 7,32,33 These results suggest that LncRNA XIST may act as a key regulator of CFA-induced inflammatory pain and SGC activation, which have the phenotypical characteristics of oligodendrocytes and astrocytes, and can promote neuron formation in DRG. Analogously, Peng et al 31 corroborated that knockdown of lncRNA NONRATT021972 inhibits hyperalgesia induced by TNF-α, SGC activation, and mechanical and thermal hyperalgesia in Type 2 diabetes mellitus rats.…”

Section: Discussionmentioning

confidence: 78%

Inhibition of lncRNA X inactivate‐specific transcript ameliorates inflammatory pain by suppressing satellite glial cell activation and inflammation by acting as a sponge of miR‐146a to inhibit Na_v1.7

Sun

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNA) has been validated to participate in nociception in inflammatory pain, presenting as a potential target against anesthesia. Previous research work confirmed the correlation between lncRNA X inactivate-specific transcript (XIST) and inflammation. However, its role in inflammatory pain is undefined. In animal pain models, voltage-gated sodium channels (VGSCs) reportedly participate in neural excitation. In this study, we observed the high expression of XIST and VGSC 1.7 (Na 1.7) in the dorsal root ganglion (DRG) of the complete Freund's adjuvant (CFA)-induced rat inflammatory pain model. Furthermore, XIST inhibition alleviated pain behavior and the activation of DRG satellite glial cells by suppressing glial fibrillary acidic protein (GFAP) expression, as well as inflammatory cytokine levels of interleukin-6 and tumor necrosis factor-α. XIST downregulation increased the mechanical pain threshold in an inflammatory pain model. Moreover, the expression of miR-146a was decreased in CFA rats. In vitro, XIST acted as a sponge of miR-146a, which targeted Na 1.7 via bioinformatic prediction, luciferase reporter, and pull-down assay. More importantly, activation of the Na 1.7 pathway or miR-146 depression both reversed XIST knockdown-inhibited satellite glial cell activation and inflammatory pain in CFA rats. These results suggest that cessation of XIST may ameliorate inflammatory pain by acting as a sponge of miR-146a to inhibit Nav1.7, implying a promising strategy against inflammatory pain.

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Recent advances in basic research on the trigeminal ganglion

Cited by 36 publications

References 28 publications

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

TFOS DEWS II pain and sensation report

Inhibition of lncRNA X inactivate‐specific transcript ameliorates inflammatory pain by suppressing satellite glial cell activation and inflammation by acting as a sponge of miR‐146a to inhibit Na_v1.7

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Recent advances in basic research on the trigeminal ganglion

Cited by 36 publications

References 28 publications

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

A pilot study of nocturnal temporalis muscle activity in TMD diagnostic groups of women

TFOS DEWS II pain and sensation report

Inhibition of lncRNA X inactivate‐specific transcript ameliorates inflammatory pain by suppressing satellite glial cell activation and inflammation by acting as a sponge of miR‐146a to inhibit Nav1.7

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Inhibition of lncRNA X inactivate‐specific transcript ameliorates inflammatory pain by suppressing satellite glial cell activation and inflammation by acting as a sponge of miR‐146a to inhibit Na_v1.7