Differential effects of SKF 38393 and LY 141865 on nociception and morphine analgesia

Ben-Sreti, M.M.; Gonzalez, J. P.; Sewell, Robert David Edmund

doi:10.1016/0024-3205(83)90590-8

Cited by 47 publications

(20 citation statements)

References 13 publications

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“…Moreover, the antinociceptive effects of apomorphine were blocked by the D2-like receptor antagonist, eticlopride [40]. In line with this, administration of a selective D2-like dopamine receptor agonist intracerebroventricularly or in the striatum produced antinociceptive effects [19,41]. Additionally, Sheng et al demonstrated that quinpirole microinjection into the ventrolateral orbital cortex produces dose-dependent and raclopride-reversible antinociception in the tail flick test [42].…”

Section: Discussionmentioning

confidence: 84%

Role of dopamine D2-like receptors within the ventral tegmental area and nucleus accumbens in antinociception induced by lateral hypothalamus stimulation

Moradi

Yazdanian

Haghparast

2015

Behavioural Brain Research

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Section: Discussionmentioning

confidence: 84%

Role of dopamine D2-like receptors within the ventral tegmental area and nucleus accumbens in antinociception induced by lateral hypothalamus stimulation

Moradi

Yazdanian

Haghparast

2015

Behavioural Brain Research

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“…For example, central dopamine depletion facilitates opioid-induced analgesia, 6 but central administration of dopamine receptor antagonists enhances nociception. [7][8][9] Moreover, Ben-Sreti et al 10 showed that a dopamine agonist that increased morphine-induced analgesia when administered centrally inhibited morphine analgesia when administered systemically. However, none of these studies examined the effects on nociception of dopamine receptor antagonists that are used routinely as antiemetics.…”

Section: Introductionmentioning

confidence: 98%

Interactions Between Metoclopramide and Morphine: Enhanced Antinociception and Motor Dysfunction in Rats

Kamerman

Becker

Fick

2006

Clin Exp Pharma Physio

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1. Opioid analgesics and anti-emetics are often used concomitantly to treat pain and nausea and vomiting in people with malignant disease. We investigated interactions between the opioid analgesic morphine and the anti-emetic metoclopramide, a dopamine D2 receptor antagonist, on nociception and gross motor function. 2. To assess for antinociceptive interactions, 11 Sprague-Dawley rats were injected intraperitoneally with morphine (5.0 mg/kg) or saline in combination with metoclopramide (0.5, 1.5 and 5.0 mg/kg) or saline and, 30 min later, the tail-flick latencies to a noxious thermal stimulus (49 degrees C water) were measured. Immediately thereafter we induced reperfusion hyperalgesia in the rats' tails using a tourniquet cuff and tested nociception again. Because, in addition to its ability to block D2 receptors, metoclopramide is also a weak 5-HT(3) receptor antagonist, we assessed in a further 11 rats whether any antinociceptive interactions occurred between morphine (5.0 mg/kg) and ondansetron (0.2 and 2.0 mg/kg), an anti-emetic that selectively antagonizes 5-HT(3) receptors. To assess for motor interactions, we injected another group of nine rats with morphine (5.0 mg/kg) or saline in combination with metoclopramide (0.5 and 5.0 mg/kg) or saline and tested the ability of the animals to run on an 80 mm diameter rod rotating at 25 r.p.m. for 30 min. 3. Metoclopramide was not inherently analgesic or antihyperalgesic, but the highest dose of metoclopramide (5.0 mg/kg) enhanced the analgesic and antihyperalgesic effects of morphine. Neither dose of ondansetron was analgesic or antihyperalgesic or enhanced the antinociceptive actions of morphine. 4. Only the high dose of metoclopramide compromised running performance when administered with saline. However, coadministering morphine with metoclopramide (both doses) decreased motor performance. 5. Therefore, metoclopramide, possibly through its actions on D2 receptors and not 5-HT(3) receptors, enhances the analgesic and antihyperalgesic effects of morphine, but morphine exacerbates metoclopramide-induced motor dysfunction in rats.

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“…Experiments in animal models have also suggested that DA activity in the nigrostriatal pathway is associated with pain suppression, an effect that appears mediated though DA D 2 receptors (Lin et al, 1981;Ben-Sreti et al, 1983;Morgan and Franklin, 1991;Altier and Stewart, 1999;Magnusson and Fisher, 2000). In this regard, the administration of levodopa, an indirect DA agonist, has been reported to reduce pain ratings in painful diabetic neuropathy in humans (Ertas et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Variations in the Human Pain Stress Experience Mediated by Ventral and Dorsal Basal Ganglia Dopamine Activity

Scott¹,

Heitzeg²,

Koeppe³

et al. 2006

J. Neurosci.

268

208

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In addition to its involvement in motor control and in encoding reward value, increasing evidence also implicates basal ganglia dopaminergic mechanisms in responses to stress and aversive stimuli. Basal ganglia dopamine (DA) neurotransmission may then respond to environmental events depending on their saliency, orienting the subsequent responses of the organism to both positive and negative stimuli. Here we examined the involvement of DA neurotransmission in the human response to pain, a robust physical and emotional stressor across species. Positron emission tomography with the DA D 2 receptor antagonist radiotracer

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Differential effects of SKF 38393 and LY 141865 on nociception and morphine analgesia

Cited by 47 publications

References 13 publications

Role of dopamine D2-like receptors within the ventral tegmental area and nucleus accumbens in antinociception induced by lateral hypothalamus stimulation

Role of dopamine D2-like receptors within the ventral tegmental area and nucleus accumbens in antinociception induced by lateral hypothalamus stimulation

Interactions Between Metoclopramide and Morphine: Enhanced Antinociception and Motor Dysfunction in Rats

Variations in the Human Pain Stress Experience Mediated by Ventral and Dorsal Basal Ganglia Dopamine Activity

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