Understanding inflammatory pain: ion channels contributing to acute and chronic nociception

Linley, John E.; Rose, Kirstin E.; Ooi, Lezanne; Gamper, Nikita

doi:10.1007/s00424-010-0784-6

Cited by 117 publications

(104 citation statements)

References 153 publications

(154 reference statements)

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“…In a previous study, Shp-1 mutant mice exhibited systemic inflammation and thermal hyperalgesia, 9 but there were no further studies on the underlying mechanisms of the thermal hyperalgesia that may be attributed to changed ion channel functions during systemic inflammation, such as TRPV1, P2X3, acid-sensing ionic channels, ATP-sensitive potassium channel (K ATP ), voltage-gated sodium channels, Kv7, etc. 14,19 In this study, intrathecal injection of Shp-1 inhibitors induced thermal hyperalgesia in naive rats, which was completely abolished by pretreatment of TRPV1 antagonists (Fig. 6A-E), implying the dependence of Shp-1 in nociception on TRPV1 activation.…”

Section: Shp-1 Inhibited the Activation Of Trpv1 And Maintained Thermsupporting

confidence: 52%

Shp-1 dephosphorylates TRPV1 in dorsal root ganglion neurons and alleviates CFA-induced inflammatory pain in rats

Xiao

Zhao

et al. 2015

Pain

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Transient receptor potential vanilloid 1 (TRPV1) receptors are expressed in nociceptive neurons of rat dorsal root ganglions (DRGs) and mediate inflammatory pain. Nonspecific inhibition of protein-tyrosine phosphatases (PTPs) increases the tyrosine phosphorylation of TRPV1 and sensitizes TRPV1. However, less is known about tyrosine phosphorylation's implication in inflammatory pain, compared with that of serine/threonine phosphorylation. Src homology 2 domain-containing tyrosine phosphatase 1 (Shp-1) is a key phosphatase dephosphorylating TRPV1. In this study, we reported that Shp-1 colocalized with and bound to TRPV1 in nociceptive DRG neurons. Shp-1 inhibitors, including sodium stibogluconate and PTP inhibitor III, sensitized TRPV1 in cultured DRG neurons. In naive rats, intrathecal injection of Shp-1 inhibitors increased both TRPV1 and tyrosine-phosphorylated TRPV1 in DRGs and induced thermal hyperalgesia, which was abolished by pretreatment with TRPV1 antagonists capsazepine, BCTC, or AMG9810. Complete Freund's adjuvant (CFA)-induced inflammatory pain in rats significantly increased the expression of Shp-1, TRPV1, and tyrosine-phosphorylated TRPV1, as well as the colocalization of Shp-1 and TRPV1 in DRGs. Intrathecal injection of sodium stibogluconate aggravated CFA-induced inflammatory pain, whereas Shp-1 overexpression in DRG neurons alleviated it. These results suggested that Shp-1 dephosphorylated and inhibited TRPV1 in DRG neurons, contributing to maintain thermal nociceptive thresholds in normal rats, and as a compensatory mechanism, Shp-1 increased in DRGs of rats with CFA-induced inflammatory pain, which was involved in protecting against excessive thermal hyperalgesia.

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Section: Shp-1 Inhibited the Activation Of Trpv1 And Maintained Thermsupporting

confidence: 52%

Shp-1 dephosphorylates TRPV1 in dorsal root ganglion neurons and alleviates CFA-induced inflammatory pain in rats

Xiao

Zhao

et al. 2015

Pain

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“…Several substances -e.g., H + , NO, K + , ATP, bradykinin (BKN), PGE 2 , NGF, TNF-, IL-6, and glutamate -are known to cause peripheral sensitization (Coutaux et al, 2005;Mense, 2009;Momin & McNaughton, 2009). The action of these substances is mediated by their specific receptors mainly found in three classes: 1) G protein coupled receptors; 2) receptor tyrosine kinases; and 3) ionotropic receptors/ion channels (Linley et al, 2010). Sensitization is often accompanied by an increase in the sensitive area (Mense, 1993).…”

Section: Muscle Nociception and Peripheral Sensitizationmentioning

confidence: 99%

Potential Muscle Biomarkers of Chronic Myalgia in Humans - A Systematic Review of Microdialysis Studies

Gerdle¹,

Larsson²

2012

Biomarker

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“…Intraplantar injection of LPS induces central sensitization that reduces the threshold for nociception in the hot-plate and other pain tests (Kanaan et al, 1996). Peripheral mechanisms are well established to play a particularly important role in inflammatory pain sensitization, which include ion channels [e.g., sensory transient receptor potential (TRP) channels, acid-sensitive channels, and P2X receptors] and proinflammatory cytokines (Linley et al, 2010). LPS-induced hyperalgesia has a relatively short duration of action and is reversible (Kanaan et al, 1996).…”

mentioning

confidence: 99%

Regulation of Inflammatory Pain by Inhibition of Fatty Acid Amide Hydrolase

Naidu¹,

Kinsey²,

Guo³

et al. 2010

J Pharmacol Exp Ther

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Although cannabinoids are efficacious in laboratory animal models of inflammatory pain, their established cannabimimetic actions diminish enthusiasm for their therapeutic development. Conversely, fatty acid amide hydrolase (FAAH), the chief catabolic enzyme regulating the endogenous cannabinoid N-arachidonoylethanolamine (anandamide), has emerged as an attractive target for treating pain and other conditions. Here, we tested WIN 55212 and CB 1 mechanisms of action. However, the transient receptor potential vanilloid type 1 antagonist capsazepine did not affect either the antihyperalgesic or antiedematous effects of URB597. Finally, URB597 attenuated levels of the proinflammatory cytokines interleukin-1␤ and tumor necrosis factor ␣ in LPS-treated paws. These findings demonstrate that simultaneous elevations in non-neuronal and neuronal endocannabinoid signaling are possible through inhibition of a single enzymatic target, thereby offering a potentially powerful strategy for treating chronic inflammatory pain syndromes that operate at multiple levels of anatomical integration.Increased pain sensitivity is one of the most common and debilitating symptoms of inflammatory disorders and is caused by various mediators, including neuropeptides, eicosanoids, and cytokines (Dray and Bevan, 1993). Cannabis extracts and cannabinoid receptor agonists have long been known to elicit analgesic and anti-inflammatory actions (Sofia et al., 1973); however, the therapeutic utility of these drugs has been greatly limited by the occurrence of psychotropic side effects. The endogenous cannabinoid (endocannabinoid) system, consisting of naturally occurring ligands (e.g., anandamide) and 2-arachidonoyl glycerol (2-AG), enzymes regulating ligand biosynthesis and degradation, and two cloned cannabinoid receptors (i.e., CB 1 and CB 2 ) (Jhaveri et al., 2007;Ahn et al., 2008), provides multiple targets for the development of new pharmacological approaches for

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Understanding inflammatory pain: ion channels contributing to acute and chronic nociception

Cited by 117 publications

References 153 publications

Shp-1 dephosphorylates TRPV1 in dorsal root ganglion neurons and alleviates CFA-induced inflammatory pain in rats

Shp-1 dephosphorylates TRPV1 in dorsal root ganglion neurons and alleviates CFA-induced inflammatory pain in rats

Potential Muscle Biomarkers of Chronic Myalgia in Humans - A Systematic Review of Microdialysis Studies

Regulation of Inflammatory Pain by Inhibition of Fatty Acid Amide Hydrolase

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