Effects of Naltrexone on Spontaneous Itch-Associated Responses in NC Mice With Chronic Dermatitis

Maekawa, Tatsuya; Yamaguchi-Miyamoto, Tomomi; Nishimura, Hiroshi; Kuraishi, Yasushi

doi:10.1254/jjp.90.193

Cited by 38 publications

(30 citation statements)

References 16 publications

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“…44) On the basis of those results, we hypothesized that biting of the regions that the rodents cannot scratch with their hind paws is an itch-associated behavioral response. In murine models of pathological pruritus, caudally directed biting was shown to be inhibited by opioid antagonists, 31,45) supporting the idea that caudally directed biting is an itch-associated behavior.…”

Section: Biting Behaviorsmentioning

confidence: 75%

“…[28][29][30] However, opioid antagonists may act on the lower brainstem rather than on the spinal dorsal horn and the periphery to inhibit itch signaling. 31,32) These findings, taken together, suggest that µ-opioid receptors are involved in the transmission or positive modulation of itch signals in the brain under normal conditions.…”

Section: Scratching Behaviors and Opioid Receptorsmentioning

confidence: 92%

“…25,51) The frequencies of spontaneous scratching of the rostral part of the body and biting of the caudal part of the body were found to be positively correlated with the spontaneous activities of the cutaneous nerves innervating the corresponding cutaneous areas. 31) This suggests that spontaneous scratching and biting are primarily due to pruriceptive inputs. Systemic administration of naltrexone inhibits spontaneous scratching and biting behaviors without affecting the increased activity of the cutaneous nerves, suggesting that the μ-opioid receptor antagonist inhibits itching by acting on the central nervous system.…”

Section: Pruriceptive Activity Of Primary Sensory Nervesmentioning

confidence: 99%

“…Systemic administration of naltrexone inhibits spontaneous scratching and biting behaviors without affecting the increased activity of the cutaneous nerves, suggesting that the μ-opioid receptor antagonist inhibits itching by acting on the central nervous system. 31) On the other hand, a single topical application of E6005, a phosphodiesterase 4 inhibitor, decreases both spontaneous scratching and the activity of the cutaneous nerves, suggesting that E6005 inhibits itching by acting primarily in the periphery. 52,53) In ICR mice, acute cutaneous allergy increased hind-paw scratching and cutaneous nerve activity, the time courses of which were similar.…”

Section: Pruriceptive Activity Of Primary Sensory Nervesmentioning

confidence: 99%

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Methods for Preclinical Assessment of Antipruritic Agents and Itch Mechanisms Independent of Mast-Cell Histamine

Kuraishi

2015

Biological & Pharmaceutical Bulletin

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Itch is a sensation that provokes a desire to scratch. Mast-cell histamine was thought to be a key itch mediator. However, histamine and mast-cell degranulation were reported not to elicit scratching in animals. It was difficult to investigate the pathophysiology of itching and to evaluate the antipruritic efficacy of chemical agents in the early 1990 s. We showed that hind-paw scratching and biting were elicited by stimulation with pruritogenic agents in mice. Those results demonstrated for the first time that cutaneous itching could be evaluated behaviorally in animals. We established various animal models of pathological itch of the skin (dry skin, mosquito allergy, surfactant-induced pruritus, and herpes zoster) and mucus membranes (pollen allergy). Mast-cell histamine did not play a key role in itching in any animal model examined except for the pollen allergy model. Histamine is not an exclusive itch mediator of mast cells; tryptase and leukotriene B 4 released from mast cells also act as itch mediators. Epidermal keratinocytes release several itch mediators, such as leukotriene B 4 , sphingosylphosphorylcholine, thromboxane A 2 , nociceptin, nitric oxide, and histamine, which may play important roles in pathological itching. Appropriate animal models of pathological itching are needed for pharmacological evaluation of the antipruritic efficacy of chemical agents.

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Section: Biting Behaviorsmentioning

confidence: 75%

Section: Scratching Behaviors and Opioid Receptorsmentioning

confidence: 92%

Section: Pruriceptive Activity Of Primary Sensory Nervesmentioning

confidence: 99%

Section: Pruriceptive Activity Of Primary Sensory Nervesmentioning

confidence: 99%

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Methods for Preclinical Assessment of Antipruritic Agents and Itch Mechanisms Independent of Mast-Cell Histamine

Kuraishi

2015

Biological & Pharmaceutical Bulletin

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“…Also the scratching movements by the hind paw was defined as a scratching bout which ended when the mice either licked its hind paw or placed its hind paw back on the floor and a series of one or more biting movements were counted as one episode which ended when the mouse returned to the straight-forward position. 16) Histopatholgical Studies The dorsal skin was isolated from each mouse, fixed in 4% paraformaldehyde solution, and stabilized in 30% sucrose solution. It was subsequently embedded in Tissue-Tek o.C.T Compound (Sakura, U.S.A.), sectioned, and stained with hematoxylin and eosin.…”

Section: Evaluation Of Skin Dermatitis Severitymentioning

confidence: 99%

Effect of Eriodictyol on the Development of Atopic Dermatitis-Like Lesions in ICR Mice

Park

Lee

Kim

2013

Biological & Pharmaceutical Bulletin

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Atopic dermatitis (AD) is a chronic, allergic, and inflammatory skin disease associated with eczema and dermatitis symptoms. Our previous studies have reported that eriodictyol extract inhibits immunoglobulin E (IgE)/Ag-induced type I hypersensitivity by suppressing the activation of proinflammatory cytokines, such as interleukin-4 (IL-4), and the expression of ceramide kinase. In this study, we investigated the inhibitory effect of eriodictyol on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in ICR mice. Treatment with 2 mg/mL eriodictyol for DNCB-induced AD-like skin lesions in ICR mice improved scratching behavior and skin severity score. Histological analysis demonstrated that thickening of the skin lesions were significantly reduced in the eriodictyol-treated group. Also, eriodictyol suppressed the DNCB-mediated elevation of IgE serum levels. These results suggest that eriodictyol may be a potential therapeutic resource for AD and an adjunctive agent to control itchiness in AD.Key words atopic dermatitis; eriodictyol; skin severity; scratching behaviorThe rate of atopic dermatitis (AD) has been increasing recently in many industrialized countries and its occurrence is usually during early infancy and childhood, but can also be in adulthood.1,2) AD is a chronic, relapsing, and inflammatory skin disease in humans and is associated with eczematous symptoms and immunoglobulin E (IgE) hyperproduction. AD is caused by a complex interrelationship among genetic, immunologic, and skin barrier dysfunction factors. 3-5)The earliest event involved in the pathogenesis of AD is considered to be a disruption of skin barrier function after scratching. Itching is a serious problem in AD patients because scratching worsens the dermatitis.6) Reduction of itching-associated scratching is the most effective therapeutic strategy for improving the quality of life for AD patients.AD is associated with the paradigm of an allergic T helper (Th) 2-mediated disease, characterized by abnormal IgE production, peripheral eosinophilia, and mast cell activation as well as upregulation of Th2 and Th1 cytokines in chronic skin lesions. 7,8) Topical steroids and immunosuppressive agents have been standard treatments for severe cases of AD. However, many patients are still worried about the long-term use of these agents and their potential adverse effects.9-11) Therefore, there is a great need for the development of new and effective therapies for AD.Eriodictyol is a unique constituent of the painted maple (Acer mono) and yerba santa (Eriodictyon californicum). Pharmacological activities attributed to eriodictyol include the control of blood vessel permeability in arthralgia and fracture, as well as antioxidant and antimicrobial effects. 12,13) Recently, our previous studies demonstrated that eriodictyol inhibits IgE-mediated allergic responses by blocking degranulation associated with ceramide kinase. Also, we showed that eriodictyol inhibits anaphylactic shock in an animal model and blocks the release of inflammatory cytokines...

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Neurobiology of Itch (Pruritus)

Akiyama

Mochizuki

Carstens

2015

Encyclopedia of Life Sciences

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Itch is often defined as an ‘unpleasant sensation that provokes the desire to scratch’. Recent studies have provided novel insights into the molecular mechanisms underlying itch‐selective signalling pathways from the periphery to the central nervous system. Chronic itch is often associated with inflammatory skin diseases such as atopic dermatitis, psoriasis or contact dermatitis, as well as systemic diseases such as renal, cholestatic, hematologic or endocrine pruritus or pruritus related to malignancy, and reduces quality of life. Chronic itch is thought to involve the sensitisation of itch‐signalling pathways, the molecular and cellular processes of which we are just starting to uncover. This review article describes recent findings regarding the basic mechanisms of itch transmission from the skin to the brain. We further describe the neuronal changes that occur both peripherally and centrally under conditions of chronic itch. Key Concepts There are a variety of endogenous pruritogens and external itch stimuli. Itch transducing channels include TRPV1, TRPA1 and Nav1.7. Spinal excitatory and inhibitory interneurons process itch information. Descending noradrenergic and serotonergic systems modulate spinal itch transmission. Sensitisation occurs in both peripheral and central nervous system under conditions of chronic itch. NK1‐expressing spinal neurons play a major role in itch sensitisation.

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Effects of Naltrexone on Spontaneous Itch-Associated Responses in NC Mice With Chronic Dermatitis

Cited by 38 publications

References 16 publications

Methods for Preclinical Assessment of Antipruritic Agents and Itch Mechanisms Independent of Mast-Cell Histamine

Methods for Preclinical Assessment of Antipruritic Agents and Itch Mechanisms Independent of Mast-Cell Histamine

Effect of Eriodictyol on the Development of Atopic Dermatitis-Like Lesions in ICR Mice

Neurobiology of Itch (Pruritus)

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