Involvement of serotonin receptors 5-HT1 and 5-HT2 in 12(S)-HPETE-induced scratching in mice

Kim, Dae-Kwon; Kim, Hyoung-June; Kim, Hyuk; Koh, Jae‐Young; Kim, Kwang-Mi; Noh, Minsoo; Kim, Jung‐Ju; Lee, Chang‐Hoon

doi:10.1016/j.ejphar.2007.11.005

Cited by 33 publications

(14 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Serotonin has been reported to be an important pruritogen in mice, because dermal mast cells in rodents contain little histamine but high concentrations of serotonin (Purcell et al, 1989). It is also reported that serotonin receptors such as 5HT1 and 5-HT2 receptors exist in the peripheral nerve endings (Kim et al, 2008a). Therefore, 5-HT from dermal mast cells and peripheral nerve endings might play an essential role in inducing ISR via serotonin receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Capsaicin, a well-known Trpv1 receptor agonist (0.005 and 0.05%) (Bevan and Szolcsanyi, 1990) was applied topically after the injection of Gsp, and naltrexone (10 mg/kg) was administered orally 1 h prior according to reports of Kim (Kim et al, 2008a). Capsaicin or naltrexone significantly suppressed the Gsp-induced scratching response in mice (Fig.…”

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

confidence: 99%

See 1 more Smart Citation

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Kim¹,

Kim²,

Noh³

et al. 2010

Biomolecules and Therapeutics

Self Cite

View full text Add to dashboard Cite

-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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

Self Cite

View full text Add to dashboard Cite

show abstract

“…Approximately 80 years ago, it was reported that intramuscular histamine injections resulted in pruritus, suggesting an important role of histamine in the pathogenesis of itching (Stander and Steinhoff, 2002). It was reported that pruritus, induced by the mast cell degranulating compound 48/80 in AD patients, could not be relieved by cetir- (Stander and Steinhoff, 2002) Serotonin ＋ Serotonin receptor 5-HT1, 5-HT2, 5-HT3 (Kim et al, 2008a;Weisshaar et al, 1997;Yamaguchi et al, 1999) TFLLR-NH2 (PAR-1), AYPGKF-NH2 (PAR-4) ＋ Histamine dependent (Tsujii et al, 2008) SLIGRL-NH2 (PAR-2) ＋ Histamine independent (Shimada et al, 2006) Acetylcholine ＋ Not known (Stander and Steinhoff, 2002) Substance P (SP) Arg-Pro-Lys-Pro-Gln-GlnPhe-Phe-Gly-Leu-Met ＋ Histamine liberator (Weidner et al, 2000) Gastrin-releasing peptides ＋ GRPR (Sun et al, 2009) Morphine ＋ Opioid receptor (Yokoyama et al, 2009) izine H1 blocker . The lack of efficacy of currently used antihistamine medicines targeting H1 and H2 receptors in AD has led to the hypothesis that mast cell mediators, other than histamine, are the cause of these conditions, or that other types of histamine receptors exist Badertscher et al, 2005).…”

Section: Inflammatory Lipidsmentioning

confidence: 99%

Progress of Pruritus Research in Atopic Dermatitis

Lee¹

2010

Biomolecules and Therapeutics

Self Cite

View full text Add to dashboard Cite

-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...

show abstract

“…Histamine is both algesic and pruritic, producing itch at the most superficial dermal/nasal/ocular level and pain when injected into deeper levels. Specific nerve cells, called pruriceptors, are responsible for propagating itch stimuli, and these are mediated by histamine H-1 and H-4 receptors [Rossbach et al 2011], as well as receptors for serotonin and protease-activated receptor 2 [Kim et al 2008]; all of these are G protein-coupled receptor (GPCR)-based pathways. These itch-responsive GPCRs trigger G protein-coupled signaling cascades, ultimately activating transient receptor potential-ion channelmediated pathways.…”

Section: The Origin Of Itchmentioning

confidence: 99%

Ocular itch associated with allergic conjunctivitis: latest evidence and clinical management

Ackerman

Smith

Gomes

2016

Therapeutic Advances in Chronic Disease

View full text Add to dashboard Cite

Allergic conjunctivitis is one of the most common allergic conditions worldwide. Its incidence is increasing due to changing climate, pollution, increased pollen loads, and the subject's heightened immunological sensitivity in response to these environmental changes. The pathophysiology predominantly involves immunoglobulin E-related mast-cell activation, with release of histamine and other mediators contributing to the propagation of the response by calling in other immune cells and further inflammation. This article presents the evolution of ocular allergy treatments, from vasoconstrictors, to antihistamines and mastcell stabilizers, to the dual-acting agents, as well as corticosteroid and immunomodulatory options. Future targets for allergy treatment are also discussed.

show abstract

Involvement of serotonin receptors 5-HT1 and 5-HT2 in 12(S)-HPETE-induced scratching in mice

Cited by 33 publications

References 20 publications

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Glucosylsphingosine Induces Itch-Scratch Responses in Mice

Progress of Pruritus Research in Atopic Dermatitis

Ocular itch associated with allergic conjunctivitis: latest evidence and clinical management

Contact Info

Product

Resources

About