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Search results for: AntiNociceptin

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#25179576   2014/08/30 To Up

Ellagic acid enhances morphine analgesia and attenuates the development of morphine tolerance and dependence in mice.

According to our previous study, ellagic acid has both dose-related central and peripheral antinociceptive effect through the opioidergic and l-arginine-NO-cGMP-ATP sensitive K(+) channel pathways. In the present study, the systemic antinociceptive effects of ellagic acid in animal models of pain, and functional interactions between ellagic acid and morphine in terms of analgesia, tolerance and dependence were investigated. Ellagic acid (1-30mg/kg; i.p.) showed significant and dose-dependent antinociceptive effects in the acetic acid-induced writhing test. Intraperitoneal ellagic acid acutely interacted with morphine analgesia in a synergistic manner in this assay. Ellagic acid (1-10mg/kg; i.p.) also exerted analgesic activity in the hot-plate test. Pre-treatment with naloxone (1mg/kg; i.p.) significantly reversed ellagic acid, morphine as well as ellagic acid-morphine combination-induced antinociceptin in these two tests. More importantly, when co-administered with morphine, ellagic acid (1-10mg/kg) effectively blocked the development of tolerance to morphine analgesia in the hot-plate test. Likewise, ellagic acid dose-dependently prevented naloxone-precipitated withdrawal signs including jumping and weight loss. Ellagic acid treatment (1-30mg/kg; i.p.) had no significant effect on the locomotion activity of animals using open-field task. Therefore, these results showed that ellagic acid has notable systemic antinociceptive activity for both tonic and phasic pain models. Altogether, ellagic acid might be used in pain relief alone or in combination with opioid drugs because of enhancing morphine analgesia and preventing morphine-induced tolerance to analgesia and dependence.
Mohammad Taghi Mansouri, Bahareh Naghizadeh, Behnam Ghorbanzadeh

1359 related Products with: Ellagic acid enhances morphine analgesia and attenuates the development of morphine tolerance and dependence in mice.

10 mg100ug 1 G10 mg100ug100ug Lyophilized96 wells (1 kit) 25 G196tests200ul

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#11108256   // To Up

Role of endogenous nociceptin in the regulation of arginine vasopressin release in conscious rats.

The effects of central administration of the opioid-like peptide nociceptin (also known as orphanin FQ) were investigated on the secretion of arginine vasopressin (AVP) in response to dehydration and hyperosmolar or hypovolemic stimulation in conscious rats. Intracerebroventricular (i.c.v.) administration of nociceptin suppressed plasma AVP concentration in a dose-dependent manner (0.1-10 microg/rat) in dehydrated rats, and the maximum effect was obtained 10 min after the administration (dehydration with 10 microg/rat nociceptin, 3.11 +/- 0.27 pg/ml vs. control, 10.32 +/- 0.96 pg/ml). The plasma AVP increase in response to either hyperosmolality [i.p. injection of hypertonic saline (HS) (600 mosml/kg)] or hypovolemia [i.p. injection of polyethylene glycol (PEG)] was also significantly blunted when nociceptin was injected i.c.v. (HS with 10 microg/rat nociceptin, 1.16 +/- 0.09 pg/ml vs. control, 1.82 +/- 0.30 pg/ml; PEG with 10 microg/rat nociceptin, 0.91 +/- 0.16 pg/ml vs. control, 2.41 +/- 0.26 pg/ml). Pretreatment with a selective opioid kappa-receptor antagonist, nor-binaltorphimine (1 microg/ rat, i.c.v.) or naloxone (2.5 mg/rat, s.c. injection) did not reverse the inhibitory effects of nociceptin on AVP release. Moreover, when plasma AVP was suppressed by acute water loading, immunoneutralization of endogenous nociceptin by antinociceptin-antiserum i.c.v. significantly reversed the suppression (0.57 +/- 0.12 pg/ml vs. control, 0.25 +/- 0.04 pg/ml). These results suggest that central nociceptin is physiologically involved in the control of AVP release through an inhibitory action.
S Kakiya, T Murase, H Arima, H Yokoi, Y Iwasaki, Y Miura, Y Oiso

2487 related Products with: Role of endogenous nociceptin in the regulation of arginine vasopressin release in conscious rats.

1300 units96 tests 100 UG96 wells

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#9098532   // To Up

Neuropeptide FF inhibition of morphine effects in the rat hippocampus.

Opioids have an excitatory effect on CA1 pyramidal neurons in the hippocampus due to the inhibition of gamma-aminobutyric acid (GABA) release from interneurons. Electrophysiologically, this pyramidal cell excitation is mainfest as an increase in extracellularly recorded population spikes, while the reduction in synaptic GABA release is manifest as a decrease in the amplitude of intracellularly recorded inhibitory postsynaptic potentials (IPSPs). Recent studies suggest that some of the behavioral effect of opioids, such as antinociceptin, can be inhibited antiopioid peptides such as neuropeptide FF (NPFF). In the present study, we have used the hippocampal response to opioids to examine the potential interactions between morphine and NPFF in vitro. Morphine alone (20-200 microM) caused reversible concentration-dependent increases in population spikes and decreases in IPSPs. In extracellular experiments, NPFF (1 microM) alone had no effect on population spikes, but significantly and concentration-dependently inhibited the morphine-induced increases in these responses. Intracellular experiments indicated that while NPFF had no effect on IPSP amplitude, or other pyramidal neurons membrane properties (membrane potential, input resistance, afterhyperpolarization, action potential frequency), it significantly reduced the decrease in IPSP amplitude caused by morphine. These results demonstrate that NPFF can attenuate the effects of morphine on population spikes and IPSPs in the hippocampus, and suggest that this effect occurs at a presynaptic site, possibly involving GABAergic interneurons.
K K Miller, C R Lupica

1496 related Products with: Neuropeptide FF inhibition of morphine effects in the rat hippocampus.

48 assays 0.1ml (1mg/ml)96 assays 148 assays

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#8930965   // To Up

Nociceptin or antinociceptin: potent spinal antinociceptive effect of orphanin FQ/nociceptin in the rat.

A heptadecapeptide (orphanin FQ or nociceptin) was recently identified as an endogenous ligand for the orphan opioid-like receptor. Here we report that intrathecal orphanin FQ produces dose-dependent depression of a spinal nociceptive flexor reflex in the rat. Furthermore, administration of orphanin FQ in rats with intrathecal catheters produced behavioural antinociception in the tail flick test with no signs of sedation or motor impairment. The reflex depressive effect of orphanin FQ was not reversed by antagonists of opioidergic, alpha 2-adrenergic and GABA-A receptors. Thus, orphanin FQ may suppress nociceptive input at the spinal level through an novel mechanism. Orphanin FQ or agonists of its receptor may represent novel analgesics for pain conditions which are not responsive to existing pharmacological therapy.
X J Xu, J X Hao, Z Wiesenfeld-Hallin

1071 related Products with: Nociceptin or antinociceptin: potent spinal antinociceptive effect of orphanin FQ/nociceptin in the rat.

1100ug

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