Opposite effects of acute versus chronic naltrexone administration on ethanol-induced locomotion

• Published in: Behavioural brain research 2004-08, Vol.153 (1), p.61-67
• Main Authors: Sanchis-Segura, Carles, Pastor, Raúl, Aragon, Carlos M.G
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Behavioral psychophysiology; Biological and medical sciences; Central Nervous System Depressants - pharmacology; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Interactions; Ethanol; Ethanol - pharmacology; Fundamental and applied biological sciences. Psychology; Locomotion; Mice; Motor Activity - drug effects; Mu opioid receptor (MOR); Naltrexone; Naltrexone - administration & dosage; Narcotic Antagonists - administration & dosage; Neurotransmission and behavior; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; β-endorphin
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2003.11.003

Several studies have pointed out that the mu opioid receptor (MOR) can play a key role in some of the behavioural effects of ethanol. In the present study, the implication of the MOR in ethanol-induced locomotion in mice was assessed. First, the effects of the administration of different naltrexone doses (0.001–1.000 mg/kg) on the locomotor changes produced by ethanol (2.5 g/kg) were evaluated. In a second set of experiments, the ability of repeated naltrexone (6 mg/kg) administrations to modify the effects of ethanol was also assessed on mice locomotion. The results of the present study revealed that an acute naltrexone administration reduced dose-dependently ethanol-induced locomotion. Conversely, after repeated naltrexone injections, a transient boost of ethanol induced locomotor activity was observed. Thus, the results of the present study revealed that the effects of these naltrexone pretreatments on ethanol-induced locomotion are similar to the previously described changes on MOR activity. Moreover, the same (acute and chronic) naltrexone pretreatments produced similar changes on the locomotion of mice after a challenge with morphine (a MOR agonist), but not after tert-butanol (an alcohol which does not release β-endorphins) administration. Therefore, our results are discussed in terms of the proved ability of ethanol to promote the release of β-endorphins and, consequently, to activate the MOR.