naloxone and Dermatitis

naloxone has been researched along with Dermatitis* in 7 studies

Other Studies

7 other study(ies) available for naloxone and Dermatitis

ArticleYear
Design and Synthesis of Enantiomerically Pure Decahydroquinoxalines as Potent and Selective κ-Opioid Receptor Agonists with Anti-Inflammatory Activity in Vivo.
    Journal of medicinal chemistry, 2017, 03-23, Volume: 60, Issue:6

    In order to develop novel κ agonists restricted to the periphery, a diastereo- and enantioselective synthesis of (4aR,5S,8aS)-configured decahydroquinoxalines 5-8 was developed. Physicochemical and pharmacological properties were fine-tuned by structural modifications in the arylacetamide and amine part of the pharmacophore as well as in the amine part outside the pharmacophore. The decahydroquinoxalines 5-8 show single-digit nanomolar to subnanomolar κ-opioid receptor affinity, full κ agonistic activity in the [

    Topics: Animals; Anti-Inflammatory Agents; Dermatitis; Drug Design; Guinea Pigs; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Inbred ICR; Quinoxalines; Rats, Wistar; Receptors, Opioid, kappa; Skin

2017
Dermatitis artefacta: psychological and neurological distress?
    La Clinica terapeutica, 2014, Volume: 165, Issue:3

    Topics: Adrenal Cortex Hormones; Dermatitis; Female; Histamine Antagonists; Humans; Male; Mental Disorders; Middle Aged; Naloxone; Pruritus; Self-Injurious Behavior

2014
Morphine directly inhibits nociceptors in inflamed skin.
    Journal of neurophysiology, 2006, Volume: 95, Issue:4

    Peripherally delivered opiates attenuate mechanical and thermal hyperalgesia in experimental models of inflammation, suggesting that activation of peripheral opioid receptors decreases the excitability of nociceptors in inflamed tissues. The current study examines the effects of peripheral morphine sulfate on response properties of sensory neurons in healthy and inflamed skin. Afferent units (185) were isolated from tibial nerve of rats using an in vitro glabrous skin-nerve teased-fiber preparation. Of these, 107 units were from normal healthy skin, and 78 were from inflamed skin 18 h after intraplantar injection of complete Freund's adjuvant. As a population, C-fiber units innervating inflamed skin exhibited properties characteristic of sensitization when compared with units innervating healthy control skin. Mechanical thresholds were lowered, responses to noxious mechanical and thermal stimuli were elevated, a greater proportion of units was spontaneously active, and the average rate of spontaneous discharge was higher. Response properties in other conduction velocity groups remained unchanged. Fifty-eight percent of C and C/Adelta nociceptors innervating inflamed skin were opiate-sensitive, and their excitability was attenuated by direct application of morphine to their receptive fields. All morphine-sensitive units were nociceptors from inflamed skin with conduction velocities <1.3 m/s. Morphine effects were concentration-dependent and naloxone-sensitive, indicating that the effects were receptor-mediated. These findings provide direct evidence that morphine acts through peripheral opioid receptors to inhibit the activity of cutaneous nociceptors under conditions of inflammation.

    Topics: Action Potentials; Animals; Dermatitis; Dose-Response Relationship, Drug; Male; Morphine; Naloxone; Narcotics; Neural Conduction; Neurons, Afferent; Nociceptors; Peripheral Nervous System; Rats; Rats, Sprague-Dawley; Receptors, Opioid; Signal Transduction; Skin

2006
Intradermal nociceptin elicits itch-associated responses through leukotriene B(4) in mice.
    The Journal of investigative dermatology, 2004, Volume: 123, Issue:1

    Nociceptin, the endogenous peptide ligand for opioid receptor like-1 (ORL1) receptor, has been implicated in the inflammation and pain in the skin. We examined whether nociceptin is a pruritogen in mice. Intradermal injections of nociceptin (1-100 nmol per site) concentration dependently increased scratching in ICR mice; the effect started within 1 min, peaked at 10-20 min, and almost subsided by 30 min. The nociceptin action was absent in ORL1 receptor-deficient (ORL1(-/-)) mice. Systemic, but not local, treatment with naloxone significantly inhibited scratching induced by nociceptin. The action of nociceptin was inhibited by the leukotriene B(4) receptor antagonist ONO-4057 and azelastine, which inhibits the action and production of leukotriene B(4) in the skin. Prepronociceptin and ORL1 receptor mRNAs were substantially expressed in the skin, whereas their expression levels were very low in the dorsal root ganglia. In the skin, nociceptin- and ORL1 receptor-like immunoreactivities were localized in the epidermis. Administration of nociceptin to primary cultures of keratinocytes from ICR and C57BL/6 (ORL1(+/+)) mice, but not ORL1(-/-) mice, produced leukotriene B(4). The results suggest that nociceptin acts on ORL1 receptor on the keratinocytes to produce leukotriene B(4), which induces itch-associated responses in mice.

    Topics: Animals; Anti-Allergic Agents; Dermatitis; Immunosuppressive Agents; Injections, Intradermal; Keratinocytes; Leukotriene B4; Male; Mice; Mice, Inbred C57BL; Mice, Inbred ICR; Mice, Mutant Strains; Naloxone; Narcotic Antagonists; Nociceptin; Nociceptin Receptor; Opioid Peptides; Phenylpropionates; Phthalazines; Protein Precursors; Pruritus; Receptors, Opioid; Terfenadine; Vasodilator Agents

2004
Effect of chronic sciatic nerve lesion on the neurogenic inflammatory response in intact and acutely injured denervated rat skin.
    Inflammation research : official journal of the European Histamine Research Society ... [et al.], 1996, Volume: 45, Issue:8

    A supersensitivity to the neuropeptide substance P (SP) has been shown to develop in post-terminal membranes of many denervated tissues. This study examined changes in the sensitivity of post-terminal vascular receptors to SP and calcitonin gene-related peptide (CGRP) in rat skin microvasculature following sciatic nerve section. In anaesthetised rats, 0.5 cm of sciatic nerve in the right mid-thigh region was removed. Two weeks later, SP (100 microM) and sodium nitroprusside (SNP, 1 mM), a direct smooth muscle vasodilator, were introduced into denervated intact footpad skin, via the electrophoresis technique. Laser doppler flowmeter was used to record changes in relative blood flow in the rat hind footpad. The results showed a significant increase in SP response over controls and slight increase in smooth muscle reactivity as determined by an increase in the vascular response to SNP. In another set of experiments, the sensitivity of post-terminal receptors was examined over a 4 weeks period in an acutely injured footpad skin of sciatic nerve lesioned rats. A vacuum-induced blister was raised on the hind footpad and SP, CGRP (each at 1 microM) or SNP (100 microM) were superfused over the blister base. In nerve lesioned rats, using the acutely injured footpad skin model, the results showed a reduction in the vascular responses to SP, CGRP and SNP. The response to SP continued to decrease over time reaching 22% of control values by 4 weeks. Responses to SNP and CGRP were reduced to 53% and 45% respectively by 2 weeks and then improved to 75% of control values by 4 weeks. Possible contributions of sympathetic efferents and the saphenous nerve to these reduced responses in acutely injured skin of nerve lesioned rats were examined using guanethidine (50 mg/kg i.p.) or sectioned saphenous nerve respectively. These procedures did not significantly modify the reduced vascular responses in the blister base of lesioned rats. Possible activation of endogenous opioids and/or the release of endothelin due to blister induction in nerve lesioned rats was examined using naloxone and the endothelin receptor antagonist, BQ-123, respectively. Treatment with naloxone increased SP response in lesioned rats to 41% of control value with no change in smooth muscle reactivity. BQ-123 significantly increased the responses to SP and SNP to 51% and 100% of their own control values respectively. It is concluded that supersensitivity of post-terminal vascular receptors develops in intac

    Topics: Anesthesia; Animals; Blister; Calcitonin Gene-Related Peptide; Denervation; Dermatitis; Electrophoresis; Endothelin Receptor Antagonists; Male; Naloxone; Narcotic Antagonists; Nitroprusside; Peptides, Cyclic; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Sciatic Nerve; Skin; Substance P; Vasodilator Agents

1996
Morphine inhibits antidromic vasodilatation without affecting the excitability of C-polymodal nociceptors in the skin of the rat.
    Brain research, 1993, Apr-02, Volume: 607, Issue:1-2

    The effect of morphine was examined under identical conditions on (a) antidromic vasodilatation, an 'efferent' function of C-nociceptors in the skin, and (b) afferent responses to heat and pressure of C-polymodal nociceptors. Morphine caused a large, naloxone-reversible, fall in peak antidromic vasodilatation (ADV). However it caused no significant change in heat or mechanical excitability of C-polymodal nociceptors in normal or mildly inflamed skin. The mechanisms by which morphine might affect efferent, but not afferent, functions of C-nociceptors are discussed.

    Topics: Action Potentials; Animals; Blood Pressure; Dermatitis; Electric Stimulation; Male; Morphine; Naloxone; Nerve Fibers; Nociceptors; Pain Threshold; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Skin; Vasodilation

1993
Effect of peripheral nerve stimulation on the dorsal horn cell activity in cats with cutaneous inflammation.
    Yonsei medical journal, 1992, Volume: 33, Issue:2

    There are some reports showing that an experience of long-enduring pain causes a change in the pain transmission system, suggesting a plastic nature of the nociceptive system. However, most of the studies concerning the analgesic effect of peripheral nerve stimulation dealt with normal animal or human subjects. So, the present study was undertaken to investigate the effect of peripheral nerve stimulation on the dorsal horn cell activity using a tonic pain model, which was made by producing a cutaneous inflammation. The main results are summarized as follows. 1) The evoked activity by electrical or natural stimulation as well as spontaneous activity was enhanced, and the receptive field size was also expanded by the inflammation. 2) Peripheral nerve conditioning stimulation reduced the C-response of the dorsal horn cell in the normal and inflamed group, and the degree of inhibition between the two groups showed no significant difference. 3) Inhibition of the C-response of the dorsal horn cells by peripheral conditioning stimulation was completely reversed by naloxone in the inflamed group whereas there was a partial block in the normal group.

    Topics: Analgesia; Animals; Cats; Dermatitis; Electric Stimulation Therapy; Endorphins; Female; Genes, fos; Male; Naloxone; Nerve Fibers; Peripheral Nerves

1992