Antinociception induced by acute oral administration of sweet substance in young and adult rodents: The role of endogenous opioid peptides chemical mediators and 渭₁-opioid receptors

详细信息	查看全文 | 推荐本文 |

• 作者：Renato Leonardo de Freitas^a ; ^b ; Joã ; o Marcus Lopes Kü ; bler^a ; Daoud Hibraim Elias-Filho^a ; ^b ; Norberto Cysne Coimbra^a ; ^b ; ^{nccoimbr@fmrp.usp.br}
• 关键词：Sweet substance-induced antinociception ; Tail-flick latencies ; Endogenous opioid peptides ; 渭1-opioid receptors
• 刊名：Pharmacology Biochemistry and Behavior
• 出版年：2012
• 期刊代码：219_00913057
• 类别：med
• 出版时间：April, 2012
• 卷：101
• 期：2
• 页码：265-270
• 文件大小：552 K

摘要

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 渭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 渭L 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 4mg/kg) of the non-selective opioid receptor antagonist naloxone, the selective 渭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 渭₁-opioid receptor actions.