Antinociception induced by acute oral administration of sweet substance in young and adult rodents: The role of endogenous opioid peptides chemical mediators and μ1-opioid receptors
ABSTRACT The present work aimed to investigate the effects of acute sucrose treatment on the perception of painful stimuli. Specifically, we sought to determine the involvement of the endogenous opioid peptide-mediated system as well as the role of the μ(1)-opioid receptor in antinociception organisation induced by acute sucrose intake. Nociception was assessed with the tail-flick test in rats (75, 150 and 250 g) of different ages acutely pre-treated with 500 μL of a sucrose solution (25, 50, 150 and 250 g/L) or tap water. Young and Adult rats (250 g) showed antinociception after treatment with 50 g/L (during 5 min) and 150 g/L and 250 g/L (during 20 min) sucrose solutions. Surprisingly, this antinociception was more consistent in mature adult rodents than in pups. To evaluate the role of opioid systems, mature adult rodents were pre-treated with different doses (0.25, 1 or 4 mg/kg) of the non-selective opioid receptor antagonist naloxone, the selective μ(1)-opioid receptor antagonist naloxonazine or vehicle followed by 250 g/L sucrose solution treatment. Sucrose-induced antinociception was reduced by pre-treatment with both naloxone and naloxonazine. The present findings suggest that sweet substance-induced hypo-analgesia is augmented by increasing sucrose concentrations in young and adult rodents. Acute oral sucrose treatment inhibits pain in laboratory animal by mediating endogenous opioid peptide and μ(1)-opioid receptor actions.
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ABSTRACT: Transcutaneous electrical nerve stimulation (TENS) is a non-pharmacological therapy for the treatment of pain. The present work investigated the effect of cannabidiol, naloxone and diazepam in combination with 10Hz and 150Hz TENS. Male Wistar rats were submitted to the tail-flick test (baseline), and each rodent received an acute administration (intraperitoneal) of naloxone (3.0mg/kg), diazepam (1.5mg/kg) or cannabidiol (0.75mg/kg, 1.5mg/kg, 3.0mg/kg, 4.5mg/kg, 6.0mg/kg and 12.0mg/kg); 10min after the acute administration, 10Hz or 150Hz TENS or a sham procedure was performed for 30min. Subsequently, tail-flick measures were recorded over a 90-min period, at 5-min intervals. 10Hz TENS increased the nociceptive threshold during the 90-min period. This antinociceptive effect was reversed by naloxone pre-treatment, was not altered by diazepam pre-treatment and was abolished by cannabidiol pre-treatment (1.5mg/kg). Moreover, 150Hz TENS increased tail-flick latencies by 35min post-treatment, which was partially inhibited by naloxone pre-treatment and totally inhibited by cannabidiol (1.5mg/kg). These data suggest the involvement of the endogenous opioid system and the cannabinoid-mediated neuromodulation of the antinociception induced by transcutaneous electrostimulation at 10Hz and 150Hz TENS.Journal of the Neurological Sciences 09/2014; 347(1-2). DOI:10.1016/j.jns.2014.09.024 · 2.26 Impact Factor
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ABSTRACT: Previous research from our laboratory has determined that in the absence of a gustatory response or taste hedonics, intraperitoneal (i.p.) glucose administration enhanced morphine-mediated analgesia in rats and had antinociceptive actions on its own. Two experiments examined the potential of a central mechanism for glucose’s actions on morphine-mediated antinociception. Morphine (2.5 μg) was infused into the periaqueductal gray (PAG) while glucose (300 mg/kg) was injected into the peritoneal cavity, or glucose (32 nmol) was infused into the PAG while morphine (3.2 mg/kg) was injected i.p. Doses of morphine and glucose were selected based on our own prior research for being below the threshold for analgesic efficacy. Antinociception was assessed using the hot-water tail-withdrawal procedure. Tailwithdrawal latency was tested at baseline (before), and 12, 24 and 36 minutes after the i.p. injection. The results indicated that 300 mg/kg glucose, administered i.p. effectively increased the antinociceptive potency of a low dose of centrally administered morphine, while central infusion of glucose enhanced peripheral morphine-mediated antinociception. These outcomes support previous evidence of glucose’s influence on the antinociception actions of opioid drugs. Furthermore, they suggest that glucose produces its enhancing actions on morphine-mediated antinociception in the brain. These results support the hypothesis that glucose does not need to go through a gustatory mechanism or taste hedonics to alter morphine’s antinociceptive actions.
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ABSTRACT: The effects of intraperitoneal (ip) d-glucose administration on antinociception were studied in male Long-Evans rats. Rats were assessed for antinociception using the hot-water tail-withdrawal procedure (54±0.2° C) to determine if peripheral administration of d-glucose (300, 560, or 720mg/kg) would enhance morphine-mediated antinociception (MMA) (1.0, 3.0, 4.2, 5.6, and 10.0mg/kg cumulative-dosing regime) and if d-glucose (560, 720, or 1000mg/kg) alone could produce antinociceptive activity that was naloxone (0.32mg/kg) reversible. Additionally, the actions of d-glucose on MMA were compared with a stereoisomer, l-glucose, which is not metabolized. The results of these studies demonstrate that peripheral administration of d-glucose significantly enhances MMA and that d-glucose alone produces antinociceptive actions that are potentially mediated by the endogenous opioid system. Furthermore, l-glucose failed to have an effect on MMA suggesting that the alterations in antinociception seen with d-glucose are not due to stressors such as osmolality or injection. The current studies provide evidence that d-glucose alteration of antinociception is not simply a response to taste or gustation.Pharmacology Biochemistry and Behavior 12/2013; 117. DOI:10.1016/j.pbb.2013.12.002 · 2.82 Impact Factor