Abstract:
:Previous studies have demonstrated that administration of nonspecific opioid antagonists such as naltrexone or naloxone reduces ethanol-induced locomotor activity in mice. However, because of their broad pharmacological profile, it remains unclear through which opioid receptor this antagonism is achieved. Therefore, the present study was aimed at further investigating the role of the different opioid receptors in ethanol-induced (2.5 g/kg) locomotion in mice. First, we compared the effect of naltrexone (0-2 mg/kg) on ethanol-induced locomotion with that of the selective delta-opioid receptor antagonist, naltrindole (0-10 mg/kg). Results of this first set of data revealed that naltrexone completely blocked this effect of ethanol at doses suggested to occupy only mu-opioid receptors, and naltrindole did not modify ethanol-induced locomotion. In a second set of experiments, we further investigated the involvement of mu-opioid receptors in ethanol-stimulated motor activity by assessing the implication of mu(1)-, mu(1/2)-, and mu(3)-opioid receptor subtypes. Results revealed that mu(1/2)-, and to a lesser extent mu(3)-, but not mu(1)-opioid receptor subtypes are involved in the psychomotor actions of ethanol. Data are discussed together with previous results which have emphasized the critical dependence of ethanol-induced motor behaviors on opioid receptors, as well as, of the integrity of beta-endorphin synthesizing neurons from the hypothalamic Arcuate Nucleus.
journal_name
Drug Alcohol Dependjournal_title
Drug and alcohol dependenceauthors
Pastor R,Sanchis-Segura C,Aragon CMdoi
10.1016/j.drugalcdep.2004.11.007keywords:
subject
Has Abstractpub_date
2005-06-01 00:00:00pages
289-95issue
3eissn
0376-8716issn
1879-0046pii
S0376-8716(04)00331-Xjournal_volume
78pub_type
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