Behavioral signs of acute pain produced by application of endothelin-1 to rat sciatic nerve

Davar, Gudarz; Hans, Guy; Fareed, Moin U.; Sinnott, Catherine J.; Strichartz, Gary R.

doi:10.1097/00001756-199807130-00025

Cited by 131 publications

(107 citation statements)

References 7 publications

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“…Newer ET A -selective antagonists that have greater bioavailability when given orally have been developed and some (e.g., ABT-627 or Atrasentan and BMS-207940) are more potent and more selective than BQ-123 (Murugesan et al 2003;Opgenorth et al 1996;Verhaar et al 2000). However, BQ-123 has been shown to effectively attenuate nocifensive behaviors and hyperalgesia when applied locally to the sciatic nerve (Davar et al 1998 3. Mean Ϯ SE heat-response thresholds of C nociceptors in nontumorbearing (control) and in tumor-bearing (cancer) mice before (baseline) and after injection of vehicle (10 l of PBS) or ET-1 (100 M in 10 l).…”

Section: Discussionmentioning

confidence: 99%

“…For example, injection of ET-1 into the plantar surface of the hind paw evoked dose-dependent hind paw licking (Gokin et al 2001;Menendez et al 2003b;Piovezan et al 2000), and application of ET-1 directly to the sciatic nerve evoked robust hind paw flinching (Davar et al 1998;Fareed et al 2000). Injection of ET-1 into the hind paw also produced tactile allodynia (Balonov et al 2006;McKelvy et al 2007), and mechanical (da Ferreira et al 1989) and heat (Menendez et al 2003b) hyperalgesia.…”

Section: Et-1-evoked Nocifensive Behaviors and Hyperalgesiamentioning

confidence: 99%

“…Numerous studies have demonstrated that injection of ET-1 into the knee or hind paw evokes nocifensive behaviors (Baamonde et al 2004;Balonov et al 2006;De-Melo et al 1998a;Ferreira et al 1989;Gokin et al 2001;McKelvy et al 2007;Menendez et al 2003b;Piovezan et al 1998Piovezan et al , 2004Verri et al 2004Verri et al , 2005, tactile allodynia (Balonov et al 2006;McKelvy et al 2007), and mechanical (da Ferreira et al 1989) and heat (Menendez et al 2003b) hyperalgesia through a mechanism involving the ET A receptors located in peripheral tissues (Baamonde et al 2004;Davar et al 1998;De-Melo et al 1998a;Fareed et al 2000;Gokin et al 2001;Menendez et al 2003b;Piovezan et al 2000). Injection of ET-1 into the skin excites C nociceptors (Gokin et al 2001;Khodorova et al 2002;Namer et al 2007) and likely contributes to ET-1-evoked nocifensive behaviors.…”

Section: Introductionmentioning

confidence: 99%

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Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Hamamoto

Khasabov

Cain

et al. 2008

Journal of Neurophysiology

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Hamamoto DT, Khasabov SG, Cain DM, Simone DA. Tumorevoked sensitization of C nonciceptos: a role for endothelin. J Neurophysiol 100: 2300 -2311, 2008. First published August 6, 2008 doi:10.1152/jn.01337.2007. Primary and metastatic cancers that effect bone are frequently associated with pain. Sensitization of primary afferent C nociceptors innervating tissue near the tumor likely contributes to the chronic pain and hyperalgesia accompanying this condition. This study focused on the role of the endogenous peptide endothelin-1 (ET-1) as a potential peripheral algogen implicated in the process of cancer pain. Electrophysiological response properties, including ongoing activity and responses evoked by heat stimuli, of C nociceptors were recorded in vivo from the tibial nerve in anesthetized control mice and mice exhibiting mechanical hyperalgesia following implantation of fibrosarcoma cells into and around the calcaneus bone. ET-1 (100 M) injected into the receptive fields of C nociceptors innervating the plantar surface of the hind paw evoked an increase in ongoing activity in both control and tumor-bearing mice. Moreover, the selective ET A receptor antagonist, BQ-123 (3 mM), attenuated tumor-evoked ongoing activity in tumor-bearing mice. Whereas ET-1 produced sensitization of C nociceptors to heat stimuli in control mice, C nociceptors in tumor-bearing mice were sensitized to heat, and their responses were not further increased by ET-1. Importantly, administration of BQ-123 attenuated tumor-evoked sensitization of C nociceptors to heat. We conclude that ET-1 at the tumor site contributes to tumor-evoked excitation and sensitization of C nociceptors through an ET A receptor mediated mechanism.

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Section: Discussionmentioning

confidence: 99%

Section: Et-1-evoked Nocifensive Behaviors and Hyperalgesiamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Hamamoto

Khasabov

Cain

et al. 2008

Journal of Neurophysiology

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“…As ET receptor blockers were found to alleviate acute and chronic pain in several animal models, it was suggested that ETs have nociceptive effects [34,53]. Pomonis et al [135] investigated the distribution of ET receptors in DRG and found that only SGCs and non-myelinating Schwann cells expressed ET B receptors, whereas neurons expressed ET A receptors (see also Ref.…”

Section: Endothelinsmentioning

confidence: 99%

Satellite glial cells in sensory ganglia: from form to function

Hanani

2005

Brain Research Reviews

648

744

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“…ET-1 is a potent vasoconstrictor that can also evoke pain sensations in rodents and humans (14,22,(27)(28)(29)(30)(31)(32)(33)(34)(35)(36). The biological effects of ET-1 are mediated by two distinct GPCRs: endothelin A receptor (ETAR) and endothelin B receptor (ETBR) (37).…”

Section: Introductionmentioning

confidence: 99%

Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1–induced pruritus

et al. 2014

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In humans, pruritus (itch) is a common but poorly understood symptom in numerous skin and systemic diseases. Endothelin 1 (ET-1) evokes histamine-independent pruritus in mammals through activation of its cognate G protein-coupled receptor endothelin A receptor (ETAR). Here, we have identified neural endothelin-converting enzyme 1 (ECE-1) as a key regulator of ET-1-induced pruritus and neural signaling of itch. We show here that ETAR, ET-1, and ECE-1 are expressed and colocalize in murine dorsal root ganglia (DRG) neurons and human skin nerves. In murine DRG neurons, ET-1 induced internalization of ETAR within ECE-1-containing endosomes. ECE-1 inhibition slowed ETAR recycling yet prolonged ET-1-induced activation of ERK1/2, but not p38. In a murine itch model, ET-1-induced scratching behavior was substantially augmented by pharmacological ECE-1 inhibition and abrogated by treatment with an ERK1/2 inhibitor. Using iontophoresis, we demonstrated that ET-1 is a potent, partially histamine-independent pruritogen in humans. Immunohistochemical evaluation of skin from prurigo nodularis patients confirmed an upregulation of the ET-1/ETAR/ECE-1/ERK1/2 axis in patients with chronic itch. Together, our data identify the neural peptidase ECE-1 as a negative regulator of itch on sensory nerves by directly regulating ET-1-induced pruritus in humans and mice. Furthermore, these results implicate the ET-1/ECE-1/ERK1/2 pathway as a therapeutic target to treat pruritus in humans.

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Behavioral signs of acute pain produced by application of endothelin-1 to rat sciatic nerve

Cited by 131 publications

References 7 publications

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Tumor-Evoked Sensitization of C Nociceptors: A Role for Endothelin

Satellite glial cells in sensory ganglia: from form to function

Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1–induced pruritus

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