scholarly journals Peripheral Antinociception Induced by Aripiprazole Is Mediated by the Opioid System

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Renata Cristina Mendes Ferreira ◽  
Ana Flávia Almeida-Santos ◽  
Igor Dimitri Gama Duarte ◽  
Daniele C. Aguiar ◽  
Fabricio A. Moreira ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Antinociceptive Effect ◽  
Opioid System ◽  
Prostaglandin E ◽  
Intraplantar Injection ◽  
Opioid Receptor Antagonist ◽  
Antinociceptive Effects ◽  
The Right

Background. Aripiprazole is an antipsychotic drug used to treat schizophrenia and related disorders. Our previous study showed that this compound also induces antinociceptive effects. The present study aimed to assess the participation of the opioid system in this effect.Methods. Male Swiss mice were submitted to paw pressure test and hyperalgesia was induced by intraplantar injection of prostaglandin E2(PGE2, 2 μg). Aripiprazole was injected 10 min before the measurement. Naloxone, clocinnamox, naltrindole, nor-binaltorphimine, and bestatin were given 30 min before aripiprazole. Nociceptive thresholds were measured in the 3rd hour after PGE2injection.Results. Aripiprazole (100 μg/paw) injected locally into the right hind paw induced an antinociceptive effect that was blocked by naloxone (50 μg/paw), a nonselective opioid receptor antagonist. The role ofμ-,δ-, andκ-opioid receptors was investigated using the selective antagonists, clocinnamox (40 μg/paw), naltrindole (15, 30, and 60 μg/paw), and nor-binaltorphimine (200 μg/paw), respectively. The data indicated that only theδ-opioid receptor antagonist inhibited the peripheral antinociception induced by aripiprazole. Bestatin (400 μg), an aminopeptidase-N inhibitor, significantly enhanced low-dose (25 μg/paw) aripiprazole-induced peripheral antinociception.Conclusion. The results suggest the participation of the opioid system viaδ-opioid receptor in the peripheral antinociceptive effect induced by aripiprazole.

scholarly journals Interactions of galanin with endomophin-2, vasopressin and oxytocin in nociceptive modulation of the trigemino-hypoglossal reflex in rats

2008 ◽  
pp. 769-776
Author(s):  
M Zubrzycka ◽  
A Janecka
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Antinociceptive Effect ◽  
Tooth Pulp ◽  
Cerebral Ventricles ◽  
Galanin Receptor ◽  
The Third ◽  
Opioid Receptor Antagonist ◽  
Pain Transmission ◽  
Δ Opioid Receptor

Galanin (GAL) is suggested to be a neuropeptide involved in pain transmission. In this study we tried to determine, whether the increase of GAL concentration in brain cells affects impulse transmission between the motor centers localized in the vicinity of the third and fourth cerebral ventricles. The experiments were carried out on rats under chloralose anesthesia. The study objectives were realized using the method allowing to record the amplitude of evoked tongue jerks (ETJ) in response to noxious tooth pulp stimulation during the perfusion of the cerebral ventricles with solutions containing tested compounds. Perfusion of the cerebral ventricles with GAL concentration-dependently inhibited the ETJ amplitude. The antinociceptive effect of GAL was blocked by a galanin receptor antagonist, galantide (GLT) and by opioid antagonists: non-selective naloxone (Nal) and μselective β-funaltrexamine (β-FNA). In contrast, a δ-opioid receptor antagonist, naltrindole (NTI) or the κ-opioid receptor antagonist, nor-binaltrophimine (nor-BNI) did not inhibit the effect of GAL. The antinociceptive effect of GAL was more pronounced when GAL was perfused in combination with other neuropeptides/neurohormones, such as endomorphin-2 (EM-2), vasopressin (AVP) and oxytocin (OT). The present results demonstrate that in the orofacial area analgesic activity is modulated by GAL, OT and AVP and that EM-2-induced antinociception involves GAL.

Slowing of intestinal transit by fat or peptide YY depends on β-adrenergic pathway

2003 ◽  
Vol 285 (6) ◽  
pp. G1310-G1316 ◽  
Author(s):  
Henry C. Lin ◽  
Corynn Neevel ◽  
Peng-Sheng Chen ◽  
Gina Suh ◽  
Jin Hai Chen
Keyword(s):  
Small Intestine ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Peptide Yy ◽  
Intestinal Transit ◽  
Adrenergic Nerve ◽  
Distal Half ◽  
Reflex Pathway ◽  
Opioid Receptor Antagonist

Although the enteric reflex pathway triggered by volume distension is known to depend on an adrenergic nerve, it is not known whether the slowing of intestinal transit by fat or peptide YY (PYY) also depends on an adrenergic pathway. The aim of this study was to test the hypotheses that the slowing of transit by fat or PYY may depend on a β-adrenergic pathway, and this adrenergic pathway may act via the serotonergic and opioid pathways previously observed for the slowing of transit by fat. Eighteen dogs were equipped with duodenal and midgut fistulas. The small intestine was compartmentalized into the proximal and distal half of gut. The role of adrenergic, serotonergic, and opioid pathways was then tested in the slowing of intestinal transit by fat, PYY, and norepinephrine. Intestinal transit results were compared as the cumulative percent marker of recovery over 30 min. We found that the slowing of transit by fat, PYY, or norepinephrine was reversed by propranolol. In addition, the slowing effect of fat was reversed by metoprolol (β1-adrenoreceptor antagonist) but not phentolamine (α-adrenoreceptor antagonist). Furthermore, norepinephrine-induced slowing of transit was reversed by ondansetron (5-HT3 receptor antagonist) or naloxone (opioid receptor antagonist). Extending these physiological results, we also found by immunohistochemistry that β1-adrenoreceptors are expressed by neurons of the intrinsic plexuses of the small intestine. We conclude that the slowing of intestinal transit by fat or PYY depends on a β-adrenergic pathway and that this adrenergic pathway acts on serotonergic and opioid pathways.

Opioid Receptors Contribute to Antinociceptive Effect of Tianeptine on Colorectal Distension-Induced Visceral Pain in Rats

Pharmacology ◽  
2017 ◽  
Vol 101 (1-2) ◽  
pp. 96-103 ◽  
Author(s):  
S. Sırrı Bilge ◽  
Fatih İlkaya ◽  
Özge Darakcı ◽  
Engin Çiftcioğlu ◽  
Ayhan Bozkurt
Keyword(s):  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Opioid Receptors ◽  
Visceral Pain ◽  
Antinociceptive Effect ◽  
Colorectal Distension ◽  
Implanted Electrodes ◽  
Opioid Receptor Antagonist ◽  
Before And After ◽  
Peripheral Opioid Receptors

Tianeptine is a clinically effective atypical antidepressant with distinct neurochemical properties. In this study, we aimed to investigate the contribution of opioid receptors in the antinociceptive effect of tianeptine on visceral pain in awake rats and to differentiate the subtype and the localization (central and/or peripheral) of these opioid receptors involved in this antinociception. Visceromotor response to noxious colorectal distension (CRD) was quantified with electromyographic recordings, obtained from previously implanted electrodes into the external oblique musculature of rats under anesthesia, before and after tianeptine administration. The opioid receptor antagonist naloxone hydrochloride (NLX) and peripherally restricted opioid receptor antagonist naloxone methiodide (NLXM) were administered intravenously 10 min before tianeptine (10 mg/kg, i.v.). The antinociceptive effect of tianeptine was abolished by NLX (1 and 2 mg/kg, i.v.), but was partially reduced by NLXM (1 and 2 mg/kg, i.v.). A µ-opioid receptor-selective dose (0.03 mg/kg, i.v.) of NLX, but not NLXM, significantly inhibited the antinociceptive effect of tianeptine. Our results suggest that antinociceptive effect of tianeptine on CRD-induced visceral nociception in rats involves the activation of both central and peripheral opioid receptors.

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