The role of transient receptor potential A 1 (TRPA1) in the development and maintenance of carrageenan-induced hyperalgesia

Bonet, Ivan José Magayewski; Fischer, Luana; Parada, Carlos Amílcar; Tambeli, Cláudia Herrera

doi:10.1016/j.neuropharm.2012.09.020

Cited by 48 publications

(41 citation statements)

References 42 publications

(52 reference statements)

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“…Because inflammation has been reported to elicit pain hypersensitivity as a result of the up-regulation of TRPV1 expression in sensory nerves and/or TRPV1 phosphorylation in peripheral tissues (Caterina et al, 2000;Kwon et al, 2014), it is possible that these TRPV1 modulations are related, in part, to the capsaicin hypersensitivity in OU regions characterized by inflammation in histological analyses. Unexpectedly, AITC application did not change rubbing time or wiping behavior after OU development despite the fact that TRPA1 sensitization has been implicated in pain hypersensitivity following inflammation and nerve injury (Bonet et al, 2013;Staaf et al, 2009). The lack of changes in AITCevoked facial grooming behavior in animal models of OUs may result from an insufficient observation time to detect nociceptive hypersensitivity to AITC.…”

Section: Discussionmentioning

confidence: 89%

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Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

Hitomi

Ono

Miyano³

et al. 2015

Journal of Neuroscience Methods

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Section: Discussionmentioning

confidence: 89%

“…The mechano-sensitive channels TRPA1, TRPV4 and Piezo2 have all been associated with mechanical hypersensitivity under conditions of inflammation and nerve injury (Alessandri-Haber et al, 2008;Bonet et al, 2013;Dubin et al, 2012). Therefore, these channels may be involved in the mechanical hypersensitivity induced by OUs.…”

Section: Discussionmentioning

confidence: 99%

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

Hitomi

Ono

Miyano³

et al. 2015

Journal of Neuroscience Methods

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“…The phytocannabinoids used in this study can also activate non-CB 1 and CB 2 receptor-dependent pathways, including TRPV1 and TRPA1 (De Petrocellis et al, 2011). However, the genetic ablation of TRPV1 appears to either promote (Helyes et al, 2007;Wang and Wang, 2013) or suppress (Szitter et al, 2010) neutrophilic inflammation, whereas genetic ablation of TRPA1 was without effect (Bonet et al, 2013;Meseguer et al, 2014), suggesting a very complex interaction of mechanisms.…”

mentioning

confidence: 83%

The Effect of Phytocannabinoids on Airway Hyper-Responsiveness, Airway Inflammation, and Cough

Makwana

Venkatasamy

Spina

et al. 2015

J Pharmacol Exp Ther

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Cannabis has been demonstrated to have bronchodilator, antiinflammatory, and antitussive activity in the airways, but information on the active cannabinoids, their receptors, and the mechanisms for these effects is limited. We compared the effects of D 9-tetrahydrocannabinol, cannabidiol, cannabigerol, cannabichromene, cannabidiolic acid, and tetrahydrocannabivarin on contractions of the guinea pig-isolated trachea and bronchoconstriction induced by nerve stimulation or methacholine in anesthetized guinea pigs following exposure to saline or the proinflammatory cytokine, tumor necrosis factor a (TNF-a). CP55940 (2-[(1R,2R,5R)-5-hydroxy-2-(3-hydroxypropyl) cyclohexyl]-5-(2-methyloctan-2-yl) phenol), a synthetic cannabinoid agonist, was also investigated in vitro. The cannabinoids were also evaluated on TNF-aand lipopolysaccharide-induced leukocyte infiltration into the lungs and citric acid-induced cough responses in guinea pigs. TNF-a, but not saline, augmented tracheal contractility and bronchoconstriction induced by nerve stimulation, but not methacholine. D 9 -Tetrahydrocannabinol and CP55940 reduced TNF-a2enhanced nerve-evoked contractions in vitro to the magnitude of saline-incubated trachea. This effect was antagonized by the cannabinoid 1 (CB 1 ) and CB 2 receptor antagonists AM251 [N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-caroxamide] and JTE907 [N-(1,3-benzodioxol-5-ylmethyl)-1,2-dihydro-7-methoxy-2-oxo-8-(pentyloxy)-3-quinolinecarboxamide], respectively. Tetrahydrocannabivarin partially inhibited the TNF-a2enhanced nerve-evoked contractions, whereas the other cannabinoids were without effect. The effect of cannabidiol and D 9-tetrahydrocannabinol together did not differ from that of the latter alone. Only -THC demonstrated effects on airway hyper-responsiveness, anti-inflammatory activity, and antitussive activity in the airways.

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“…12 Intriguingly, TRPA1 is crucially implicated in inflammatory pain and hypersensitivity of the formalin model. [17][18][19] The pro-nociceptive action of Nocistatin in these pain paradigms has so far been attributed to attenuation of inhibitory neurotransmission in the spinal cord 12 and/or facilitation of neurotransmitter release from a population of capsaicin-sensitive (and therefore TRPV1-expressing) peripheral sensory neurons. 25 It is noteworthy that a large subset of capsaicin-sensitive TRPV1-positive sensory neurons also expresses TRPA1 channels.…”

Section: Discussionmentioning

confidence: 99%

“…in the sensory processing areas of the spinal cord). [12][13][14][15] Since the formalin model also involves sensory neurons of the peripheral nervous system and TRPA1 channels expressed in nociceptors play a crucial role for formalin-induced inflammatory pain and hypersensitivity, [17][18][19] we asked whether Nocistatin might affect TRPA1 physiology.…”

Section: Nocistatin Specifically Sensitizes Trpa1 Responses In Sensormentioning

confidence: 99%

Nocistatin sensitizes TRPA1 channels in peripheral sensory neurons

et al. 2016

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The ability of sensory neurons to detect potentially harmful stimuli relies on specialized molecular signal detectors such as transient receptor potential (TRP) A1 ion channels. TRPA1 is critically implicated in vertebrate nociception and different pain states. Furthermore, TRPA1 channels are subject to extensive modulation and regulation -processes which consequently affect nociceptive signaling. Here we show that the neuropeptide Nocistatin sensitizes TRPA1-dependent calcium influx upon application of the TRPA1 agonist mustard oil (MO) in cultured sensory neurons of dorsal root ganglia (DRG). Interestingly, TRPV1-mediated cellular calcium responses are unaffected by Nocistatin. Furthermore, Nocistatin-induced TRPA1-sensitization is likely independent of the Nocistatin binding partner 4-Nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1) as assessed by siRNA-mediated knockdown in DRG cultures. In conclusion, we uncovered the sensitization of TRPA1 by Nocistatin, which may represent a novel mechanism how Nocistatin can modulate pain.

show abstract

The role of transient receptor potential A 1 (TRPA1) in the development and maintenance of carrageenan-induced hyperalgesia

Cited by 48 publications

References 42 publications

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

The Effect of Phytocannabinoids on Airway Hyper-Responsiveness, Airway Inflammation, and Cough

Nocistatin sensitizes TRPA1 channels in peripheral sensory neurons

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