Characterizations of sphingosylphosphorylcholine-induced scratching responses in ICR mice using naltrexon, capsaicin, ketotifen and Y-27632

Kim, Hyoung June; Kim, Hyuk; Han, Eun-Sil; Park, Sun-Mi; Koh, Jae‐Young; Kim, Kwang-Mi; Noh, Minsoo; Kim, Jung‐Ju; Lee, Chang‐Hoon

doi:10.1016/j.ejphar.2008.01.005

Cited by 22 publications

(31 citation statements)

References 30 publications

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“…2). It was found that, at the same concentration, Gsp elicits scratching to the less extent as histamine, LPA or SPC (Inagaki et al, 2000;Hashimoto et al, 2004;Kim et al, 2008c). Incidentally, the reason that high amounts of Gsp are required to provoke the scratch response in ICR mice might be the weak binding affinity of the putative Gsp receptor in mice or due to nonspecific binding to endogenous proteins such as albumin in mice (Han et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

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Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Kim¹,

Kim²,

Noh³

et al. 2010

Biomolecules and Therapeutics

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-Pruritus is one of major symptoms in atopic dermatis. The pathophysiological mechanism of pruritus is unclear. The search for pruritogen is important in elucidating the pathophysiological mechanism of pruritus in atopic dermatitis. Glucosylsphingosine (Gsp) is upregulated in the strateum corneum of atopic dermatitis patients. We investigated to determine whether Gsp induces itch-scratch responses (ISRs) in mice. Intradermal administration of Gsp induces ISRs. Gsp dose-dependently induced scratching response at 50-500 nmol/site range. Pretreatment with naltrexone, an opioid μ receptor antagonist, and capsaicin, a TrpV1 receptor agonist, inhibited Gsp-induced ISRs. Additionally, Gsp-induced ISRs were also suppressed by cyproheptadine, an antagonist of serotonin receptor. These findings suggest that Gsp-induced scratching might be at least partly mediated by capsaicin-sensitive primary afferents, and the opioids receptor systems might be involved in transmission of itch signaling in the central nervous system. Furthermore, our findings suggest that Gsp-induced ISRs may be attributable to the serotonin-mediated pathways and Gsp is not any more one of byproducts of abnormal skin barrier but can lead to induce pruritus, one of typical symptoms of atopic dermatitis.

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Section: Discussionmentioning

confidence: 99%

“…Ketotifen (10 mg/kg) was applied orally 1hr before the injection of Gsp, and cyproheptadine (10 mg/kg) was injected intravenously 5 minute prior according to reports of Kim (Kim et al, 2008c).…”

Section: Effect Of Capsaicin and Naltrexone On Gsp-induced Scratchingmentioning

confidence: 99%

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Kim¹,

Kim²,

Noh³

et al. 2010

Biomolecules and Therapeutics

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“…[34][35][36] Naturally occurring d-erythro SPc, but not l-threo SPc, induces scratching after intradermal injection, raising the possibility that SPC acts on a specific receptor to induce itching. 33) However, SPc receptors remain unclear, although some candidates were reported. It is expected that the suppression of the increased activity of sphingomyelin glucosylceramide deacylase results in not only the decrease in SPc (relieving itch) but also the increase in ceramides in the stratum corneum and epidermis (improving skin dryness and barrier disruption) in patients with atopic dermatitis.…”

Section: Lipid Mediatorsmentioning

confidence: 99%

“…32) Intradermal injection of SPc, but not of sphingomyelin and sphingosine, elicits scratching in mice. [32][33][34] SPc may act on the epidermal keratinocytes, dendritic cells, primary sensory neurons, and mast cells in the skin. [34][35][36] Naturally occurring d-erythro SPc, but not l-threo SPc, induces scratching after intradermal injection, raising the possibility that SPC acts on a specific receptor to induce itching.…”

Section: Lipid Mediatorsmentioning

confidence: 99%

Potential New Therapeutic Targets for Pathological Pruritus

Kuraishi

2013

Biological & Pharmaceutical Bulletin

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Very few approved medications are indicated for the treatment of pruritus, and drug development for pruritic diseases is awaited. During the past two decades, progress has been made in understanding the molecular basis of the physiology and pathophysiology of pruritus. Newly identified potential targets for pathological pruritus include receptors (histamine H 4 receptor, leukotriene B 4 receptors, interleukin-31 receptor A, bombesin BB 2 receptor, toll-like receptor 3, α-adrenoceptor, and opioid μ-and κ-receptors), channels (transient receptor potential (TRP) V3 and TRPA1 channels), and enzymes (histidine decarboxylase, sphingomyelin glucosylceramide deacylase, 5-lipoxygenase, leukotriene A 4 hydrolase, and autotaxin). The development of specific, effective blockers and agonists/antagonists of these targets is awaited.

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“…Thus we tested whether sphingosylphosphorylcholine induces scratching response. We found that SPC dose-dependently induces scratching response in mice and these responses were specific for D-erythro-form SPC (Kim et al, 2008c;Kim et al, 2009). Andoh et al reported that LTB4 from keratinocytes mediates sphingosylphosphorylcholine-induced itch-associated responses in mouse skin (Andoh et al, 2009).…”

Section: Inflammatory Lipidsmentioning

confidence: 93%

Progress of Pruritus Research in Atopic Dermatitis

Lee¹

2010

Biomolecules and Therapeutics

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-Atopic dermatitis is a common skin disease affecting up to 10% of children and approximately 2% of adults. Atopic dermatitis exhibits four major symptoms, including intense itching, dry skin, redness and exudation. The "itch-scratch-itch" cycle is one of the major features in atopic dermatitis. The pathophysiology and neurobiology of pruritus is unclear. Currently there are no single and universally effective pharmacological antipruritic drugs for treatment of atopic dermatitis. Thus, controlling of itch is a very important unmet need in patients suffering from atopic dermatitis. This article will update progress during the past 10 years of research in the field of pruritus of atopic dermatitis, focusing on aspects of pruritogens (including inflammatory lipids, histamine, serotonin, proteinases, proteinase-activating receptors, neurotransmitters, neuropeptides, and opioid peptides), antipruritic therapies, and emerging new targets. Based on recent progress, researchers expect to identify exciting possibilities for improved treatments and to develop new antipruritic drugs acting through novel targets, such as histamine H4 receptor, gastrin-releasing peptide receptor, MrgprA3, thromboxane A2 receptor and the putative SPC receptor. Keywords: Pruritus, Atopic dermatitis, Pruritogen, Antipruritic therapy, New targetAtopic dermatitis (AD) is a common skin disease that affects up to 10% of children and approximately 2% of adults in the general population (Leung and Soter, 2001). The socio-economic losses resulting from the disease are high; the cost of illness to the third-party payer for AD ranges from US $0.9 billion to US $3.8 billion (Ellis et al., 2002). The quality-of-life is remarkably lowered by AD. The genetic background, in combination with several environmental factors, results in this chronic remittent skin disease. AD exhibits four major symptoms including intense itching (pruritus), dry skin (xerosis), redness (erythema) and exudation. The "itch-scratch-itch" cycle is a common feature of AD. Scratching can cause bleeding, secondary infection (bacterial, fungal and/or viral) and thickening of the skin (lichenification) (Lewis-Jones, 2005). Itching is the predominant symptom of AD and is also an important diagnostic feature of systemic disease (Malekzad et al., 2009).The pathophysiology and neurobiology of pruritus are unclear. Therefore it is not surprising that anti-pruritus therapy is not well established and the choice of therapeutic agents is limited. However, recent progress over the past 10 years has provided insights into the neurophysiology of pruritus and is opening up exciting possibilities for development of new antipruritic drugs (Yosipovitch and Papoiu, 2008;Liu et al., 2009;Sun et al., 2009).Itch can be regarded as a cutaneous sensory perception, which requests excitation of specialized itch receptors in the skin. Increased amounts of neurofilament-, protein gene product (PGP) 9.5-, calcitonin gene-related peptide (CGRP)-, and substance P (SP)-positive nerve fibres have been observe...

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Characterizations of sphingosylphosphorylcholine-induced scratching responses in ICR mice using naltrexon, capsaicin, ketotifen and Y-27632

Cited by 22 publications

References 30 publications

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Potential New Therapeutic Targets for Pathological Pruritus

Progress of Pruritus Research in Atopic Dermatitis

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