uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
The nociceptin/orphanin FQ receptor agonist Ro 64-6198 reduces alcohol self-administration and prevents relapse-like alcohol drinking
Department of Clinical Neuroscience, Division of Drug Dependence Research, Karolinska Institutet, Stockholm, Sweden.
Laboratory of the Biology of Addictive Diseases, The Rockefeller University, New York, NY, USA.
Department of Clinical Neuroscience, Division of Drug Dependence Research, Karolinska Institutet, Stockholm, Sweden. (Molecular neuropsychopharmacology)
Department of Clinical Neuroscience, Division of Drug Dependence Research, Karolinska Institutet, Stockholm, Sweden.
2007 (English)In: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 32, no 4, p. 902-10Article in journal (Refereed) Published
Abstract [en]

Effects of the opioid receptor like-1 (ORL-1) receptor agonist Ro 64-6198 (0.1, 0.3, and 1.0 mg/kg intraperitoneally (i.p.)) on operant ethanol self-administration and activation of self-administration by ethanol deprivation were studied in male Wistar rats. Acute administration of Ro 64-6198 caused a dose-dependent reduction of ethanol self-administration. In comparison, the opioid antagonist naltrexone (0.1, 0.3, and 1.0 mg/kg i.p.) inhibited ethanol self-administration at all doses tested. Ethanol deprivation for 10 days significantly increased ethanol self-administration during the first 2 days after deprivation. Daily pretreatment with Ro 64-6198 (0.3 mg/kg) or naltrexone (0.3 mg/kg) during the last 3 days of ethanol deprivation abolished the deprivation-induced increase in ethanol intake. Thus, stimulation of the ORL-1 receptors by Ro 64-6198 reduced the acute reinforcing effects of ethanol and prevented relapse-like behavior in the ethanol-deprivation model in a similar manner as a blockade of opioid receptors by naltrexone. Ro 64-6198 at 0.1 and 0.3 mg/kg doses did not alter self-administration of 0.2% saccharin solution, indicating an apparent selectivity of this compound in modification of ethanol reward. These findings add further support to the idea that Ro 64-6198 and potentially other synthetic ORL-1 receptor agonists are as effective as naltrexone in blocking the actions of ethanol important for its addictive potential in animal experiments, and therefore may have therapeutic value in the treatment of alcoholism.

Place, publisher, year, edition, pages
2007. Vol. 32, no 4, p. 902-10
Keyword [en]
ethanol, reward, relapse, Ro 64-6198, NBHZ, naltrexone
National Category
Pharmacology and Toxicology
Identifiers
URN: urn:nbn:se:uu:diva-120088DOI: 10.1038/sj.npp.1301169PubMedID: 16880770OAI: oai:DiVA.org:uu-120088DiVA, id: diva2:302458
Available from: 2010-03-08 Created: 2010-03-07 Last updated: 2018-01-12

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMed

Authority records BETA

Bakalkin, Georgy

Search in DiVA

By author/editor
Bakalkin, Georgy
In the same journal
Neuropsychopharmacology
Pharmacology and Toxicology

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 358 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf