Comparison of the effects of sumatriptan and the NK1 antagonist CP-99,994 on plasma extravasation in dura mater and c-fos mRNA expression in trigeminal nucleus caudalis of rats

Shepheard, Sara L.; Williamson, David J.; Williams, John T.; Hill, Ray; Hargreaves, RJ

doi:10.1016/0028-3908(94)00153-j

Cited by 161 publications

(78 citation statements)

References 16 publications

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“…A variety of reasons have been proposed for the presumed mismatch between the preclinical effects of NK1 receptor antagonists in animal models and their effects in humans including using animal species with different pain pathways to humans and differences in pharmacokinetic parameters [35,36]. Preclinical studies have shown that NK1 receptor antagonists block the neurogenic inflammatory response produced by administration of capsaicin [37,38] and electrical stimulation of the trigeminal ganglion [39]. Most of the interest surrounding the use of NK1 receptor antagonists in cough has been restricted to their involvement in the cough response in asthma [40].…”

Section: Introductionmentioning

confidence: 99%

An update and systematic review on drug therapies for the treatment of refractory chronic cough

Ryan

Vertigan

Birring

2018

Expert Opinion on Pharmacotherapy

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Introduction: Chronic Cough (CC) is common and often associated with significant comorbidity and decreased quality of life. In up to 50% of cases, the cough is refractory despite extensive investigation and treatment trials. It is likely that the key abnormality in refractory CC is dysfunctional, hypersensitive sensory nerves, similar to conditions such as laryngeal hypersensitivity and neuropathic pain.Areas covered: The aim of this systematic review is to assess drug therapies for refractory CC. The authors review the current management of CC and provide discussion of the similarities between neuropathic pain and refractory CC. They review repurposed and new pharmacological treatments. Several meta-analyses were performed to compare the efficacy of treatments where possible.Expert opinion: Repurposed pain medications such as gabapentin and pregabalin reduce the frequency of cough and improve quality of life. Along with speech pathology, they are important and alternate treatments for refractory CC. However, more treatments are needed and the P2X3 ion channel receptor antagonists show the most promise. With a better understanding of neuronal activation and sensitisation and their signal processing in the brain, improved animal models of cough, and the use of validated cough measurement tools, more effective treatments will develop.

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Section: Introductionmentioning

confidence: 99%

An update and systematic review on drug therapies for the treatment of refractory chronic cough

Ryan

Vertigan

Birring

2018

Expert Opinion on Pharmacotherapy

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“…In the periphery, triptans prevent or block neurogenic inflammation (Moskowitz, 1993;Bolay et al, 2002), at least in part, by inhibiting the release of substance P (SP) and CGRP from peptidergic afferents (Buzzi et al, 1991). There is also evidence for a central action of triptans (Kaube et al, 1993;Shepheard et al, 1995), including presynaptic regulation of neurotransmitter release from the central terminals of primary afferents in the trigeminal nucleus caudalis (Jennings et al, 2004;Levy et al, 2004), postsynaptic regulation of the responses of caudalis neurons to glutamate or an NMDA agonist (Goadsby et al, 2001), and activation of triptan receptors expressed by pain-modulatory neurons in the periaqueductal gray (Bartsch et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Tissue Injury Regulates Serotonin 1D Receptor Expression: Implications for the Control of Migraine and Inflammatory Pain

Ahn

Basbaum²

2006

J. Neurosci.

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The anti-migraine action of "triptan" drugs involves the activation of serotonin subtype 1D (5-HT 1D ) receptors expressed on "painresponsive" trigeminal primary afferents. In the central terminals of these nociceptors, the receptor is concentrated on peptidergic dense core vesicles (DCVs) and is notably absent from the plasma membrane. Based on this arrangement, we hypothesized that in the resting state the receptor is not available for binding by a triptan, but that noxious stimulation of these afferents could trigger vesicular release of DCVs, thus externalizing the receptor. Here we report that within 5 min of an acute mechanical stimulus to the hindpaw of the rat, there is a significant increase of 5-HT 1D -immunoreactivity (IR) in the ipsilateral dorsal horn of the spinal cord. We suggest that these rapid immunohistochemical changes reflect redistribution of sequestered receptor to the plasma membrane, where it is more readily detected. We also observed divergent changes in 5-HT 1D -IR in inflammatory and nerve-injury models of persistent pain, occurring at least in part through the regulation of 5-HT 1D -receptor gene expression. Finally, we found that 5-HT 1D -IR is unchanged in the spinal cord dorsal horn of mice with a deletion of the gene encoding the neuropeptide substance P. This result differs from that reported for the Ѩ-opioid receptor, which is also sorted to DCVs, but is greatly reduced in preprotachykinin mutant mice. We suggest that a "pain"-triggered regulation of 5-HT 1D -receptor expression underlies the effectiveness of triptans for the treatment of migraine. Moreover, the widespread expression of 5-HT 1D receptor in somatic nociceptive afferents suggests that triptans could, in certain circumstances, treat pain in nontrigeminal regions of the body.

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“…There is evidence, however, that they a ect the release of neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) from peripheral endings of trigeminal a erents. 5-HT 1 receptor agonists were shown to inhibit the increase of CGRP concentration in the venous out¯ow from the head both after experimental trigeminal ganglion stimulation and during migraine attacks (Buzzi et al, 1991;Goadsby & Edvinsson, 1993 and to suppress the expression of cfos in the trigeminal brain stem after noxious stimulation of trigeminal structures (Cutrer et al, 1995;Nozaki et al, 1992;Shepheard et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Release of immunoreactive substance P in the brain stem upon stimulation of the cranial dura mater with low pH – inhibition by the serotonin (5‐HT₁) receptor agonist CP 93,129

Meßlinger¹,

Ebersberger²,

Schaible³

1998

British J Pharmacology

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1 The therapeutical bene®t of serotonin (5-HT 1 ) receptor agonists in the treatment of migraine headache has been attributed to their inhibitory e ect on the release of pro-in¯ammatory neuropeptides from trigeminal a erents within the cranial meninges. The e ect of 5-HT 1 receptor agonists on the release of neuropeptides from central a erent terminals has not been examined so far. In the present study in the rat we therefore measured the e ect of the 5-HT 1B receptor agonist CP 93,129 on the stimulation-evoked release of immunoreactive substance P (ir-SP) in the spinal trigeminal nucleus. 2 To measure release of ir-SP, microprobes coated with antibody to substance P were inserted into the medulla oblongata at the level of the obex. The ipsilateral parietal dura mater encephali was exposed and stimulated with acid phosphate bu ered Tyrode solution (pH 5.8). This chemical stimulus increased the release of ir-SP in the medullary dorsal horn. 3 Systemic (i.v.) administration of CP 93,129 (460 nmol kg 71 ) prior to stimulation suppressed the stimulation-evoked increase of release of ir-SP. Local administration of CP 93,129 (10 mM) to the dorsal surface of the medulla had no signi®cant inhibitory e ect on the release. 4 It is concluded that systemically applied 5-HT 1 receptor agonists reduce the stimulation-evoked release of substance P from the central endings of meningeal a erents in the spinal trigeminal nucleus (medullary dorsal horn). This inhibitory e ect may contribute to the antinociceptive e ect of 5-HT 1 receptor agonists in migraine.

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Comparison of the effects of sumatriptan and the NK1 antagonist CP-99,994 on plasma extravasation in dura mater and c-fos mRNA expression in trigeminal nucleus caudalis of rats

Cited by 161 publications

References 16 publications

An update and systematic review on drug therapies for the treatment of refractory chronic cough

An update and systematic review on drug therapies for the treatment of refractory chronic cough

Tissue Injury Regulates Serotonin 1D Receptor Expression: Implications for the Control of Migraine and Inflammatory Pain

Release of immunoreactive substance P in the brain stem upon stimulation of the cranial dura mater with low pH – inhibition by the serotonin (5‐HT₁) receptor agonist CP 93,129

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Comparison of the effects of sumatriptan and the NK1 antagonist CP-99,994 on plasma extravasation in dura mater and c-fos mRNA expression in trigeminal nucleus caudalis of rats

Cited by 161 publications

References 16 publications

An update and systematic review on drug therapies for the treatment of refractory chronic cough

An update and systematic review on drug therapies for the treatment of refractory chronic cough

Tissue Injury Regulates Serotonin 1D Receptor Expression: Implications for the Control of Migraine and Inflammatory Pain

Release of immunoreactive substance P in the brain stem upon stimulation of the cranial dura mater with low pH – inhibition by the serotonin (5‐HT1) receptor agonist CP 93,129

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Release of immunoreactive substance P in the brain stem upon stimulation of the cranial dura mater with low pH – inhibition by the serotonin (5‐HT₁) receptor agonist CP 93,129