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Acetate causes alcohol hangover headache in rats.

By Christina R Maxwell, Rebecca Jay Spangenberg, Jan B Hoek, Stephen D Silberstein and Michael L Oshinsky

Abstract

BACKGROUND: The mechanism of veisalgia cephalgia or hangover headache is unknown. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache. METHODS: We used a chronic headache model to examine how pure ethanol produces increased sensitivity for nociceptive behaviors in normally hydrated rats. RESULTS: Ethanol initially decreased sensitivity to mechanical stimuli on the face (analgesia), followed 4 to 6 hours later by inflammatory pain. Inhibiting alcohol dehydrogenase extended the analgesia whereas inhibiting aldehyde dehydrogenase decreased analgesia. Neither treatment had nociceptive effects. Direct administration of acetate increased nociceptive behaviors suggesting that acetate, not acetaldehyde, accumulation results in hangover-like hypersensitivity in our model. Since adenosine accumulation is a result of acetate formation, we administered an adenosine antagonist that blocked hypersensitivity. DISCUSSION: Our study shows that acetate contributes to hangover headache. These findings provide insight into the mechanism of hangover headache and the mechanism of headache induction

Topics: Thomas Jefferson University, Department of Neurology, Department of Pathology, Anatomy and Cell Biology, Acetaldehyde, Acetates, Alcohol Drinking, Alcoholic Intoxication, Analgesia, Animals, Chronic Disease, Ethanol, Headache, Hypersensitivity, Inflammation, Male, Nociceptors, Rats, Rats, Sprague-Dawley, Touch, Rats, Sprague-Dawley, Biological Phenomena, Cell Phenomena, and Immunity, Medical Cell Biology, Medical Neurobiology, Neurology
Publisher: Jefferson Digital Commons
Year: 2010
OAI identifier: oai:jdc.jefferson.edu:neurologyfp-1044

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