Relationship between the catecholamine and protein content in the submaxillary salivary gland tissues of and mucosa over the secretory cycle for chronic inflammation of the oral soft tissues

Mikhailov, Valery V.; Rusanova, A. G.

doi:10.1007/bf00805140

Cited by 2 publications

(2 citation statements)

References 2 publications

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“…Although our data do not exclude actions by other isozymes of PKC, that the epsilon isozyme alone, of PKC, is responsible is supported by the observations that the prolonged response to inflammatory mediators was totally prevented by injection of a specific PKC⑀ inhibitor and that the injection of a PKC⑀ agonist alone resulted in a similar prolonged hyperalgesic response. PKC⑀ is known also to contribute to acute nociception, specifically to acute hyperalgesia produced by epinephrine (Khasar et al, 1999a,b), which may be present at increased levels during inflammation (Cunha et al, 1991;Mikhailov and Rusanova, 1993). That there is a different function of PKC⑀ in prolonged hyperalgesia compared with acute nociception is suggested by the chronic (Ͼ24 hr) nature of the resultant hyperalgesia and the apparent novel coupling of PKC⑀ to the PGE 2 receptor, a phenomenon not seen in acute hyperalgesia produced by PGE 2 (Levine and Reichling, 1999).…”

Section: Discussionmentioning

confidence: 99%

Chronic Hypersensitivity For Inflammatory Nociceptor Sensitization Mediated by the ε Isozyme of Protein Kinase C

et al. 2000

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We have identified a mechanism, mediated by the epsilon isozyme of protein kinase C (PKCepsilon) in peripheral neurons, which may have a role in chronic inflammatory pain. Acute inflammation, produced by carrageenan injection in the rat hindpaw, produced mechanical hyperalgesia that resolved by 72 hr. However, for up to 3 weeks after carrageenan, injection of the inflammatory mediators prostaglandin E(2) or 5-hydroxytryptamine or of an adenosine A(2) agonist into the same site induced a markedly prolonged hyperalgesia (>24 hr compared with 5 hr or less in control rats not pretreated with carrageenan). A nonselective inhibitor of several PKC isozymes and a selective PKCepsilon inhibitor antagonized this prolonged hyperalgesic response equally. Acute carrageenan hyperalgesia could be inhibited by PKA or PKG antagonists. However, these antagonists did not inhibit development of the hypersensitivity to inflammatory mediators. Our findings indicate that different second messenger pathways underlie acute and prolonged inflammatory pain.

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Section: Discussionmentioning

confidence: 99%

Chronic Hypersensitivity For Inflammatory Nociceptor Sensitization Mediated by the ε Isozyme of Protein Kinase C

et al. 2000

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“…Activation of ERKs by ␤-adrenergic receptor stimulation may contribute to inflammatory pain, because increased levels of epinephrine are found at sites of inflammation (Mikhailov and Rusanova, 1993) and ␤-adrenergic receptor antagonists reduce inflammatory hyperalgesia (Cunha et al, 1991). Catecholamines released from sympathetic nerve terminals and from the adrenal medulla also appear to contribute to sympathetically maintained pain and stress-aggravated pain (Choi and Rowbotham, 1997; Figure 3.…”

Section: Discussionmentioning

confidence: 99%

Nociceptor Sensitization by Extracellular Signal-Regulated Kinases

et al. 2001

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Inflammatory pain, characterized by a decrease in mechanical nociceptive threshold (hyperalgesia), arises through actions of inflammatory mediators, many of which sensitize primary afferent nociceptors via G-protein-coupled receptors. Two signaling pathways, one involving protein kinase A (PKA) and one involving the epsilon isozyme of protein kinase C (PKCepsilon), have been implicated in primary afferent nociceptor sensitization. Here we describe a third, independent pathway that involves activation of extracellular signal-regulated kinases (ERKs) 1 and 2. Epinephrine, which induces hyperalgesia by direct action at beta(2)-adrenergic receptors on primary afferent nociceptors, stimulated phosphorylation of ERK1/2 in cultured rat dorsal root ganglion cells. This was inhibited by a beta(2)-adrenergic receptor blocker and by an inhibitor of mitogen and extracellular signal-regulated kinase kinase (MEK), which phosphorylates and activates ERK1/2. Inhibitors of G(i/o)-proteins, Ras farnesyltransferases, and MEK decreased epinephrine-induced hyper-algesia. In a similar manner, phosphorylation of ERK1/2 was also decreased by these inhibitors. Local injection of dominant active MEK produced hyperalgesia that was unaffected by PKA or PKCepsilon inhibitors. Conversely, hyperalgesia produced by agents that activate PKA or PKCepsilon was unaffected by MEK inhibitors. We conclude that a Ras-MEK-ERK1/2 cascade acts independent of PKA or PKCepsilon as a novel signaling pathway for the production of inflammatory pain. This pathway may present a target for a new class of analgesic agents.

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Relationship between the catecholamine and protein content in the submaxillary salivary gland tissues of and mucosa over the secretory cycle for chronic inflammation of the oral soft tissues

Cited by 2 publications

References 2 publications

Chronic Hypersensitivity For Inflammatory Nociceptor Sensitization Mediated by the ε Isozyme of Protein Kinase C

Chronic Hypersensitivity For Inflammatory Nociceptor Sensitization Mediated by the ε Isozyme of Protein Kinase C

Nociceptor Sensitization by Extracellular Signal-Regulated Kinases

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