Potential therapeutic targets for neurokinin-1 receptor antagonists

Duffy, Ruth A.

doi:10.1517/14728214.9.1.9

Cited by 59 publications

(11 citation statements)

References 108 publications

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“…The use of modulators or blockers of SP receptors has been recently suggested [6], but further evidence is required to fully characterise the benefit/risk ratio of these molecules. Although many studies show the antinociceptive effects of NK1 receptor antagonists, several clinical trials have failed to demonstrate the analgesic efficacy of these compounds in humans [42, 43], though they have been successful in the treatment of other diverse conditions, including depression, chemotherapy-induced emesis, and inflammatory bowel disease [44]. Future studies are necessary to evaluate the usefulness of NK1 receptor antagonists to treat dental pain.…”

Section: Discussionmentioning

confidence: 99%

Peripheral Mechanisms of Dental Pain: The Role of Substance P

Sacerdote

Levrini

2012

Mediators of Inflammation

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Current evidence supports the central role of neuropeptides in the molecular mechanisms underlying dental pain. In particular, substance P, a neuropeptide produced in neuron cell bodies localised in dorsal root and trigeminal ganglia, contributes to the transmission and maintenance of noxious stimuli and inflammatory processes. The major role of substance P in the onset of dental pain and inflammation is increasingly being recognised. Well-grounded experimental and clinical observations have documented an increase in substance P concentration in patients affected by caries, pulpitis, or granulomas and in those undergoing standard orthodontic or orthodontic/dental care procedures. This paper focuses on the role of substance P in the induction and maintenance of inflammation and dental pain, in order to define future lines of research for the evaluation of therapeutic strategies aimed at modulating the complex effects of this mediator in oral tissues.

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Section: Discussionmentioning

confidence: 99%

Peripheral Mechanisms of Dental Pain: The Role of Substance P

Sacerdote

Levrini

2012

Mediators of Inflammation

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“…Notably there appears to be a relationship between postoperative ileus and intestinal inflammation (Rychter and Clave, 2013), and these conditions could be closely related with regards to a potential impact to potentiate PONV or PDNV. Antiemetics used to control PONV are also anti-inflammatory, for example, dexamethasone and 5-HT 3 and NK 1 receptor antagonists (Duffy, 2004; Faerber et al, 2007; Takao et al, 1995). …”

Section: Stimulimentioning

confidence: 99%

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

Horn¹,

Wallisch²,

Homanics³

et al. 2014

European Journal of Pharmacology

203

130

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Clinical research shows that postoperative nausea and vomiting (PONV) is caused primarily by the use of inhalational anesthesia and opioid analgesics. PONV is also increased by several risk predictors, including a young age, female sex, lack of smoking, and a history of motion sickness. Genetic studies are beginning to shed light on the variability in patient experiences of PONV by assessing polymorphisms of gene targets known to play roles in emesis (serotonin type 3, 5-HT3; opioid; muscarinic; and dopamine type 2, D2, receptors) and the metabolism of antiemetic drugs (e.g., ondansetron). Significant numbers of clinical trials have produced valuable information on pharmacological targets important for controlling PONV (e.g., 5-HT3 and D2), leading to the current multi-modal approach to inhibit multiple sites in this complex neural system. Despite these significant advances, there is still a lack of fundamental knowledge of the mechanisms that drive the hindbrain central pattern generator (emesis) and forebrain pathways (nausea) that produce PONV, particularly the responses to inhalational anesthesia. This gap in knowledge has limited the development of novel effective therapies of PONV. The current review presents the state of knowledge on the biological mechanisms responsible for PONV, summarizing both preclinical and clinical evidence. Finally, potential ways to advance the research of PONV and more recent developments on the study of postdischarge nausea and vomiting (PDNV) are discussed.

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“…For example, neurokinin-1 (NK1) receptor antagonists are expected to treat IBS and migraine because NK1 receptors are observed in GI tract as well as in CNS 111. Gabapentin, an antiepileptic, has been an alternative or combined agent to support the migraine treatment but with less level of evidence based 112.…”

Section: Treatmentsmentioning

confidence: 99%

Irritable Bowel Syndrome and Migraine: Bystanders or Partners?

Chang¹,

Lu²

2013

J Neurogastroenterol Motil

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Irritable bowel syndrome (IBS) and migraine are distinct clinical disorders. Apart from the characteristics of chronic and recurrent pain in nature, these pain-related disorders apparently share many similarities. For example, IBS is female predominant with community prevalence about 5-10%, whereas that of migraine is 1-3% also showing female predominance. They are often associated with many somatic and psychiatric comorbidities in terms of fibromyaglia, chronic fatigue syndrome, interstitial cystitis, insomnia and depression etc., even the IBS subjects may have coexisted migraine with an estimated odds ratio of 2.66. They similarly reduce the quality of life of victims leading to the social, medical and economic burdens. Their pathogeneses have been somewhat addressed in relation to biopsychosocial dysfunction, heredity, genetic polymorphism, central/visceral hypersensitivity, somatic/cutaneous allodynia, neurolimbic pain network, gonadal hormones and abuses etc. Both disorders are diagnosed according to the symptomatically based criteria. Multidisciplinary managements such as receptor target new drugs, melantonin, antispasmodics, and psychological drugs and measures, complementary and alternatives etc. are recommended to treat them although the used agents may not be necessarily the same. Finally, the prognosis of IBS is pretty good, whereas that of migraine is less fair since suicide attempt and stroke are at risk. In conclusion, both distinct chronic pain disorders to share many similarities among various aspects probably suggest that they may locate within the same spectrum of a pain-centered disorder such as central sensitization syndromes. The true pathogenesis to involve these disorders remains to be clarified in the future.

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Potential therapeutic targets for neurokinin-1 receptor antagonists

Cited by 59 publications

References 108 publications

Peripheral Mechanisms of Dental Pain: The Role of Substance P

Peripheral Mechanisms of Dental Pain: The Role of Substance P

Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting

Irritable Bowel Syndrome and Migraine: Bystanders or Partners?

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