Activation of the endogenous nociceptin system by selective nociceptin receptor agonist SCH 221510 produces antitransit and antinociceptive effect: a novel strategy for treatment of diarrhea-predominant IBS

2014 ◽  
Vol 26 (11) ◽  
pp. 1539-1550 ◽  
Author(s):  
J. Fichna ◽  
M. Sobczak ◽  
A. Mokrowiecka ◽  
A. I. Cygankiewicz ◽  
P. K. Zakrzewski ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Antinociceptive Effect ◽  
Novel Strategy ◽  
Nociceptin Receptor

scholarly journals Blockade of Adrenal Medulla-Derived Epinephrine Potentiates Bee Venom-Induced Antinociception in the Mouse Formalin Test: Involvement of Peripheralβ-Adrenoceptors

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Suk-Yun Kang ◽  
Dae-Hyun Roh ◽  
Hyun-Woo Kim ◽  
Ho-Jae Han ◽  
Alvin J. Beitz ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Formalin Test ◽  
Late Phase ◽  
Antinociceptive Effect ◽  
Bee Venom ◽  
Pain Models ◽  
Adrenergic Antagonists ◽  
Novel Strategy ◽  
Chronic Pain Conditions

The injection of diluted bee venom (DBV) into an acupoint has been used traditionally in eastern medicine to treat a variety of inflammatory chronic pain conditions. We have previously shown that DBV had a potent antinociceptive efficacy in several rodent pain models. However, the peripheral mechanisms underlying DBV-induced antinociception remain unclear. The present study was designed to investigate the role of peripheral epinephrine on the DBV-induced antinociceptive effect in the mouse formalin assay. Adrenalectomy significantly enhanced the antinociceptive effect of DBV during the late phase of the formalin test, while chemical sympathectomy had no effect. Intraperitoneal injection of epinephrine blocked this adrenalectomy-induced enhancement of the DBV-induced antinociceptive effect. Moreover, injection of a phenylethanolamine N-methyltransferase (PNMT) inhibitor enhanced the DBV-induced antinociceptive effect. Administration of nonselectiveβ-adrenergic antagonists also significantly potentiated this DBV-induced antinociception, in a manner similar to adrenalectomy. These results demonstrate that the antinociceptive effect of DBV treatment can be significantly enhanced by modulation of adrenal medulla-derived epinephrine and this effect is mediated by peripheralβ-adrenoceptors. Thus, DBV acupoint stimulation in combination with inhibition of peripheralβ-adrenoceptors could be a potentially novel strategy for the management of inflammatory pain.

Involvement of GABAA receptor-associated chloride channels in the peripheral antinociceptive effect induced by GABAA receptor agonist muscimol

2007 ◽  
Vol 564 (1-3) ◽  
pp. 112-115 ◽  
Author(s):  
Glaucia Reis ◽  
Daniela Pacheco ◽  
Janetti Francischi ◽  
Maria Castro ◽  
Andréa Perez ◽  
...  
Keyword(s):  
Gabaa Receptor ◽  
Chloride Channels ◽  
Receptor Agonist ◽  
Antinociceptive Effect

scholarly journals Buprenorphine C7‐Esters with Improved Nociceptin Receptor Agonist Potency as Analgesics

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Keith Mathew Olson ◽  
Gerta Cami‐Kobeci ◽  
Stephen M. Husbands ◽  
John R. Traynor
Keyword(s):  
Receptor Agonist ◽  
Nociceptin Receptor

scholarly journals Descending antinociception induced by secondary somatosensory cortex stimulation in experimental neuropathy: role of the medullospinal serotonergic pathway

2017 ◽  
Vol 117 (3) ◽  
pp. 1200-1214 ◽  
Author(s):  
Boriss Sagalajev ◽  
Hanna Viisanen ◽  
Hong Wei ◽  
Antti Pertovaara
Keyword(s):  
Somatosensory Cortex ◽  
Receptor Agonist ◽  
Dynamic Range ◽  
Antinociceptive Effect ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Secondary Somatosensory Cortex ◽  
Underlying Mechanisms ◽  
Wdr Neurons ◽  
Stimulation Of

Stimulation of the secondary somatosensory cortex (S2) has attenuated pain in humans and inflammatory nociception in animals. Here we studied S2 stimulation-induced antinociception and its underlying mechanisms in an experimental animal model of neuropathy induced by spinal nerve ligation (SNL). Effect of S2 stimulation on heat-evoked limb withdrawal latency was assessed in lightly anesthetized rats that were divided into three groups based on prior surgery and monofilament testing before induction of anesthesia: 1) sham-operated group and 2) hypersensitive and 3) nonhypersensitive (mechanically) SNL groups. In a group of hypersensitive SNL animals, a 5-HT1A receptor agonist was microinjected into the rostroventromedial medulla (RVM) to assess whether autoinhibition of serotonergic cell bodies blocks antinociception. Additionally, effect of S2 stimulation on pronociceptive ON-cells and antinociceptive OFF-cells in the RVM or nociceptive spinal wide dynamic range (WDR) neurons were assessed in anesthetized hypersensitive SNL animals. S2 stimulation induced antinociception in hypersensitive but not in nonhypersensitive SNL or sham-operated animals. Antinociception was prevented by a 5-HT1A receptor agonist in the RVM. Antinociception was associated with decreased duration of heat-evoked response in RVM ON-cells. In spinal WDR neurons, heat-evoked discharge was delayed by S2 stimulation, and this antinociceptive effect was prevented by blocking spinal 5-HT1A receptors. The results indicate that S2 stimulation suppresses nociception in SNL animals if SNL is associated with tactile allodynia-like hypersensitivity. In hypersensitive SNL animals, S2 stimulation induces antinociception mediated by medullospinal serotonergic pathways acting on the spinal 5-HT1A receptor, and partly through reduction of the RVM ON-cell discharge. NEW & NOTEWORTHY Stimulation of S2 cortex, but not that of an adjacent cortical area, induced descending heat antinociception in rats with the spinal nerve ligation-induced model of neuropathy. Antinociception was bilateral, and it involved suppression of pronociceptive medullary cells and activation of serotonergic pathways that act on the spinal 5-HT1A receptor. S2 stimulation failed to induce descending antinociceptive effect in sham-operated controls or in nerve-ligated animals that had not developed mechanical hypersensitivity.

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