Effect of interleukin-1β on the release of substance P from rat isolated spinal cord
References (27)
Interleukin-1 and interleukin-1 antagonism
Blood
(1991)- et al.
Interleukin-1β-induced increase in substance P in rat myenteric plexus
Gastroenterology
(1993) - et al.
The possible role of glia in nociceptive processing and hyperalgesia in the spinal cord of the rat
Neuropharmacology
(1994) - et al.
Interleukin-1 induces analgesia in mice by a central action
Eur. J. Pharmacol.
(1988) - et al.
Intracerebroventricular injection of interleukin-1 β enhances nociceptive neuronal responses of the trigeminal nucleus caudalis in rats
Brain Res.
(1994) - et al.
Indomethacin blocks central nociceptive effects of PGF2α
Brain Res.
(1986) - et al.
Characterization of cytokine-induced hyperalgesia
Brain Res.
(1994) - et al.
Cytokine-to-brain communication: a review and analysis of alternative mechanisms
Life Sci.
(1995) - et al.
Effect of bradykinin and prostaglandins on the release of calcitonin gene-related peptide-like immunoreactivity from the rat spinal cord in vitro
Br. J. Pharmacol.
(1993) - et al.
Human interleukin (IL) 1α, murine IL-1α and murine IL-1β are transported from blood to brain in the mouse by a shared saturable mechanism
J. Pharmacol. Exp. Ther.
(1991)
Blood-borne interleukin-1α is transported across the endothelial blood-spinal cord barrier of mice
J. Physiol. (London)
The involvement of bradikinin B1 and B2 receptor mechanisms in cytokine-induced mechanical hyperalgesia in the rat
Br. J. Pharmacol.
Primary structure and functional expression from complementary DNA of a human interleukin-1 receptor antagonist
Nature
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Involvement of microglial cells in the antinociceptive effects of metamizol in a mouse model of neuropathic pain
2018, Pharmacology Biochemistry and BehaviorCitation Excerpt :The chosen pronociceptive factors undoubtedly play an important role in the process of nociception (Mika et al., 2013; Popiolek-Barczyk and Mika, 2016). IL-1β is known to be strongly activated upon neural damage (Hopkins and Rothwell, 1995; Mika et al., 2008), and intrathecal administration of IL-1β induces hypersensitivity in rats (Malcangio et al., 1996; Mika et al., 2008; Obreja et al., 2002; Oprée, 2000). Moreover, IL-1β is capable of inducing secretion of other pronociceptive cytokines, including CCL2.
Maraviroc reduces neuropathic pain through polarization of microglia and astroglia - Evidence from in vivo and in vitro studies
2016, NeuropharmacologyCitation Excerpt :Overproduction of IL-1β, IL-18 and IL-6 is implicated in the pathophysiological changes that occur during different disease states, including neuropathic pain (Dinarello, 1996; Okamoto et al., 2001; Braddock and Quinn, 2004; Miyoshi et al., 2008; Ren and Torres, 2009; Pilat et al., 2015, 2016; Rojewska et al., 2016). Moreover, intrathecal administration of both IL-1β and IL-18 cause allodynia and hyperalgesia in rats (Malcangio et al., 1996; Mika et al., 2008; Miyoshi et al., 2008). In contrast, IL-1RA (Malcangio et al., 1996; Mika et al., 2008; Pilat et al., 2015) and IL-18BP promote antiallodynic activity (Miyoshi et al., 2008; Pilat et al., 2016) under conditions of neuropathy.
IL-1 receptor antagonist improves morphine and buprenorphine efficacy in a rat neuropathic pain model
2015, European Journal of PharmacologyFibromyalgia and cytokines
2014, Immunology LettersCitation Excerpt :IL-1 and TNF act synergically and induce the synthesis of adhesion molecules by endothelial cells, which are essential in neutrophil recruitment to the inflammation site. IL-1 alone, or in combination with TNF increases prostaglandin synthesis (i.e. PGE2) and regulates substance P gene expression decreasing pain threshold in peripheral nerves [17]. Patients injected with IL-1 develop fever, headache, myalgia and arthralgia and this is reduced by the administration of COX inhibitors [18] and also such symptoms are very often found in fibromyalgia patients.
Importance of glial activation in neuropathic pain
2013, European Journal of Pharmacology
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Present address: Department of Pharmacology, Queen Mary and Westfield College, Mile End Road, London E1 4NS, UK.
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Present address: Department of Pharmacology, The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.