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Pain. 2019 Jan 11. doi: 10.1097/j.pain.0000000000001482. [Epub ahead of print]

Hedonic drinking engages a supra-spinal inhibition of thermal nociception in adult rats.

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Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Republic of Korea.
Nuffield Department of Clinical Neuroscience, John Radcliffe Hospital, Oxford University, United Kingdom (current address).
Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Republic of Korea.
School of Physiology, Pharmacology & Neuroscience, Medical Sciences Building, University of Bristol, United Kingdom.
Anaesthesia, Pain & Critical Care Sciences, Translational Health Sciences, Bristol Medical School, Bristol Royal Infirmary, University of Bristol, United Kingdom.


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 (i.e. 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 appear to operate via 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 euovolaemic 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 supra-spinal 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 supra-spinal control of pain by appetite and reward.

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