Hedonic drinking engages a supraspinal inhibition of thermal nociception in adult rats
Hedonic drinking engages a supraspinal inhibition of thermal nociception in adult rats
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DOI：
10.1097/j.pain.0000000000001482
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发表时间：
2019-05-01
期刊：
影响因子：
7.4
通讯作者：
Oh, Seog Bae
中科院分区：
文献类型：
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作者：
Davies, Alexander J.;Kim, Doyun;Oh, Seog Bae
蔗糖的味道通常用于为新生儿提供疼痛缓解，并且对新生啮齿动物具有天生的镇痛作用。在成年期，蔗糖仍然是进食的强烈动力，即使在潜在的危险情况下（即组织损伤的威胁）。然而，这种内源性奖赏-疼痛相互作用的神经生物学机制尚不清楚。我们已经在Sprague-Dawley大鼠（6-10周龄）中开发了一种蔗糖饮料诱导的镇痛的简单模型，并使用后爪热敏感性的Hargreaves试验进行了行为和药理学表征。我们的研究结果揭示了一种急性，有效的，和强大的抑制作用的蔗糖饮用热伤害性行为，不像在新生儿的现象是独立的内源性阿片类药物信号转导，似乎不通过经典的脊髓回路的下行抑制。饮用蔗糖的经验具有调节作用，即蔗糖的明显预期使水单独（在等容动物中）引起短暂的安慰剂样镇痛作用。然而，单独的甜味不足以引起成年大鼠口服蔗糖灌注的镇痛作用。相反，蔗糖镇痛现象只出现在慢性插管动物经口灌注后的条件反射。这种蔗糖镇痛作用被内源性大麻素CB 1受体拮抗剂利莫那班的全身给药完全阻止。这些结果表明，存在一个内源性脊髓上的镇痛电路，这是由奖励饮酒的背景下，依赖于内源性大麻素信号。我们建议，这种享乐的蔗糖饮用模型可能是有用的，进一步调查的食欲和奖励的脊髓上的疼痛控制。
The taste of sucrose is commonly used to provide pain relief in newborn humans and is innately analgesic to neonatal rodents. In adulthood, sucrose remains a strong motivator to feed, even in potentially hazardous circumstances (ie, threat of tissue damage). However, the neurobiological mechanisms of this endogenous reward-pain interaction are unclear. We have developed a simple model of sucrose drinking-induced analgesia in Sprague-Dawley rats (6-10 weeks old) and have undertaken a behavioral and pharmacological characterization using the Hargreaves' test of hind-paw thermal sensitivity. Our results reveal an acute, potent, and robust inhibitory effect of sucrose drinking on thermal nociceptive behaviour that unlike the phenomenon in neonates is independent of endogenous opioid signalling and does not seem to operate through classical descending inhibition of the spinal cord circuitry. Experience of sucrose drinking had a conditioning effect whereby the apparent expectancy of sucrose enabled water alone (in euvolemic animals) to elicit a short-lasting placebo-like analgesia. Sweet taste alone, however, was insufficient to elicit analgesia in adult rats intraorally perfused with sucrose. Instead, the sucrose analgesia phenomenon only appeared after conditioning by oral perfusion in chronically cannulated animals. This sucrose analgesia was completely prevented by systemic dosing of the endocannabinoid CB1 receptor antagonist rimonabant. These results indicate the presence of an endogenous supraspinal analgesic circuit that is recruited by the context of rewarding drinking and is dependent on endocannabinoid signalling. We propose that this hedonic sucrose-drinking model may be useful for further investigation of the supraspinal control of pain by appetite and reward.