Development of inflammation after application of mustard oil or glutamate to the rat temporomandibular joint

Fiorentino, Paolo M; Cairns, Brian E.; Hu, James W.

doi:10.1016/s0003-9969(98)00095-8

Cited by 47 publications

(15 citation statements)

References 13 publications

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“…Topical application of MO produces neurogenic inflammation [24] and [26] and a concurrent heat and mechanical hyperalgesia [35], presumably via a centrally mediated sensitization process. Several studies have shown that these effects are TRPA1-mediated [3], [6], [30], [37] and [39].…”

Section: Resultsmentioning

confidence: 99%

Differential ATF3 expression in dorsal root ganglion neurons reveals the profile of primary afferents engaged by diverse noxious chemical stimuli

Bráz

Basbaum

2010

Pain

136

116

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Although transgenic and knockout mice have helped delineate the mechanisms of action of diverse noxious compounds, it is still difficult to determine unequivocally the subpopulations of primary afferent nociceptor that these molecules engage. As most noxious stimuli lead to tissue and/or nerve injury, here we used induction of activating transcription factor 3 (ATF3), a reliable marker of nerve injury, to assess the populations of primary afferent fibers that are activated after peripheral administration of noxious chemical stimuli. In wild-type mice, hindpaw injections of capsaicin, formalin, mustard oil or menthol induce expression of ATF3 in distinct subpopulations of sensory neurons. Interestingly, even though these noxious chemicals are thought to act through subtypes of transient receptor potential (TRP) channels, all compounds also induced ATF3 in neurons that appear not to express the expected TRP channel subtypes. On the other hand, capsaicin failed to induce ATF3 in mice lacking TRPV1, indicating that TRPV1 is required for both the direct and indirect induction of ATF3 in sensory neurons. By contrast, only low doses of formalin or mustard oil failed to induce ATF3 in TRPA1 null mice, indicating that injections of high doses (>0.5%) of formalin or mustard oil recruit both TRPA1 and non-TRPA1 expressing primary afferent fibers. Finally, peripheral injection of menthol, a TRPM8 receptor agonist, induced ATF3 in a wide variety of sensory neurons, but in a TRPM8-independent manner. We conclude that purportedly selective agonists can activate a heterogeneous population of sensory neurons, which ultimately could contribute to the behavioral responses evoked.

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Section: Resultsmentioning

confidence: 99%

Differential ATF3 expression in dorsal root ganglion neurons reveals the profile of primary afferents engaged by diverse noxious chemical stimuli

Bráz

Basbaum

2010

Pain

136

116

View full text Add to dashboard Cite

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“…Several investigations have found no or little evidence to support glutamate’s participation in vasodilation or plasma extravasation. Administration of glutamate to rat knee joint, subcutaneous skin, or TMJ does not cause noticeable redness, edema, or heat beyond vehicle controls (Coggeshall et al, 1997; Lawand et al, 1997; Cairns et al, 1998; Fiorentino et al, 1999). Intra-articular injection of MK-801 (0.3–1.5 mM, 40 μl), AP7 (0.2 mM, 100 μl), CNQX (0.1 mM, 100 μl), or NBQX (0.25–2.5 mM, 40 μl) does not decrease knee joint edema produced by carrageenan or kaolin/carrageenan injection (Lawand et al, 1997; Zhang et al, 2003).…”

Section: Peripheral Effects Of Glutamate: Biophysicalmentioning

confidence: 87%

Glutamate pharmacology and metabolism in peripheral primary afferents: Physiological and pathophysiological mechanisms

Miller

Hoffman

Sutharshan

et al. 2011

Pharmacology & Therapeutics

124

129

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In addition to using glutamate as a neurotransmitter at central synapses, many primary sensory neurons release glutamate from peripheral terminals. Primary sensory neurons with cell bodies in dorsal root or trigeminal ganglia produce glutaminase, the synthetic enzyme for glutamate, and transport the enzyme in mitochondria to peripheral terminals. Vesicular glutamate transporters fill neurotransmitter vesicles with glutamate and they are shipped to peripheral terminals. Intense noxious stimuli or tissue damage causes glutamate to be released from peripheral afferent nerve terminals and augmented release occurs during acute and chronic inflammation. The site of action for glutamate can be at the autologous or nearby nerve terminals. Peripheral nerve terminals contain both ionotropic and metabotropic excitatory amino acid receptors (EAARs) and activation of these receptors can lower the activation threshold and increase the excitability of primary afferents. Antagonism of EAARs can reduce excitability of activated afferents and produce antinociception in many animal models of acute and chronic pain. Glutamate injected into human skin and muscle causes acute pain. Trauma in humans, such as arthritis, myalgia, and tendonitis, elevates glutamate levels in affected tissues. There is evidence that EAAR antagonism at peripheral sites can provide relief in some chronic pain sufferers.

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“…Some authors have suggested the induction of TMJ arthritis surgically [29–32] or mechanically [33], using a systemic injection of heat-inactivated group A Streptococcus pyogenes [34] or an injection in submandibular lymph nodes with Mycobacterium cells [35]. However, other models consisting of an intra-articular injection of inflammatory substances, such as NaCI, KC1, histamine [2], mustard oil [3, 4], substance P [5], heat-killed Mycobacterium butyricum in paraffin oil [6], human recombinant IL-1 α [7, 8], glutamate [9], ovalbumin antigen [10], complete Freund's adjuvant [11, 12], formalin [13], capsaicin [14], or carrageenan [15–17], have been used previously.…”

Section: Discussionmentioning

confidence: 99%

Experimental Model of Zymosan‐Induced Arthritis in the Rat Temporomandibular Joint: Role of Nitric Oxide and Neutrophils

Chaves

Ribeiro

Souza

et al. 2011

BioMed Research International

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Aims. To establish a new model of zymosan-induced temporomandibular joint (TMJ) arthritis in the rat and to investigate the role of nitric oxide. Methods. Inflammation was induced by an intra-articular injection of zymosan into the left TMJ. Mechanical hypernociception, cell influx, vascular permeability, myeloperoxidase activity, nitrite levels, and histological changes were measured in TMJ lavages or tissues at selected time points. These parameters were also evaluated after treatment with the nitric oxide synthase (NOS) inhibitors L-NAME or 1400 W. Results. Zymosan-induced TMJ arthritis caused a time-dependent leucocyte migration, plasma extravasation, mechanical hypernociception, and neutrophil accumulation between 4 and 24 h. TMJ immunohistochemical analyses showed increased inducible NOS expression. Treatment with L-NAME or 1400 W inhibited these parameters. Conclusion. Zymosan-induced TMJ arthritis is a reproducible model that may be used to assess both the mechanisms underlying TMJ inflammation and the potential tools for therapies. Nitric oxide may participate in the inflammatory temporomandibular dysfunction mechanisms.

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Development of inflammation after application of mustard oil or glutamate to the rat temporomandibular joint

Cited by 47 publications

References 13 publications

Differential ATF3 expression in dorsal root ganglion neurons reveals the profile of primary afferents engaged by diverse noxious chemical stimuli

Differential ATF3 expression in dorsal root ganglion neurons reveals the profile of primary afferents engaged by diverse noxious chemical stimuli

Glutamate pharmacology and metabolism in peripheral primary afferents: Physiological and pathophysiological mechanisms

Experimental Model of Zymosan‐Induced Arthritis in the Rat Temporomandibular Joint: Role of Nitric Oxide and Neutrophils

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