Increasing sympathetic nerve terminal-dependent plasma extravasation correlates with decreased arthritic joint injury in rats
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Dioclea violacea lectin ameliorates inflammation in the temporomandibular joint of rats by suppressing intercellular adhesion molecule-1 expression
2019, BiochimieCitation Excerpt :Therefore, the development of new drugs to treat inflammatory diseases from orofacial tissues continues to be of considerable importance to scientists. After tissue and/or neural damage the inflammatory response induces the local release of inflammatory chemical mediators, which in turn promote the inflammatory chemotaxis characterized by plasma extravasation and neutrophil migration [8]. Neutrophil is the main leukocyte involved in the host defense, whose intense influx into the injured tissue has been associated with the development and chronicity of inflammatory diseases, such as TMD [9].
Neurogenic Regulation of Bradykinin-Induced Synovitis
2009, NeuroImmune BiologyCitation Excerpt :The role of the sympathetic postganglionic neuron in inflammation has been most extensively studied in the synovium (see Ref. [16] for review). For example, selective activation of the sympathetic postganglionic neuron terminal with 6-hydroxydopamine, to displace sympathetic neurotransmitters from vesicular stores [70,71], increases plasma extravasation in the rat knee joint [72], and plasma extravasation is decreased by surgical [73–79] or chemical (with guanethidine or 6-hydroxydopamine) [72,80–89] sympathectomy. In particular, surgical or chemical sympathectomy attenuates the magnitude of both basal plasma extravasation and that induced by bradykinin, a principal inflammatory mediator, in the rat knee joint by 60–70% [88,90,91] and producing a large leftward shift in the dose–response curve for bradykinin (Fig. 2).
Peripheral Sympathetic Component of the Temporomandibular Joint Inflammatory Pain in Rats
2006, Journal of PainCitation Excerpt :In addition to prostaglandins, sympathomimetic amines such as norepinephrine are also released at the site of inflammation,20,33 where they contribute to the inflammatory hyperalgesia.2,27 Therefore, our finding that depletion of intracellular stores of norepinephrine by guanethidine significantly attenuated the TMJ hyperalgesia induced by carrageenan indicates that norepinephrine contributes to the hyperalgesic state in the TMJ, as previously demonstrated in other tissues.14,15,16,33,46 This finding is consistent with the dense innervation of the temporomandibular joint by sympathetic fibers arising from cells of the superior cervical ganglion28,50,51 from where norepinephrine may be released.
Sympathetic neurotransmitters in joint inflammation
2005, Rheumatic Disease Clinics of North AmericaThe importance of timing of adrenergic drug delivery in relation to the induction and onset of adjuvant-induced arthritis
2004, Brain, Behavior, and Immunity
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Present address: Pain Mechanisms Laboratory, Neuroscience Group, Clinical Research Institute of Montreal, Montreal, Québec, Canada H2W 1R7.