Ibudilast reduces alcohol drinking in multiple animal models of alcohol dependence

Neuroinflammatory signaling pathways in the central nervous system are of current interest as potential pharmacotherapy targets for alcohol dependence. In this study, we examined the ability of ibudilast, a non‐selective phosphodiesterase inhibitor, to reduce alcohol drinking and relapse in alcohol‐...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Addiction biology 2015-01, Vol.20 (1), p.38-42
Hauptverfasser: Bell, Richard L., Lopez, Marcelo F., Cui, Changhai, Egli, Mark, Johnson, Kirk W., Franklin, Kelle M., Becker, Howard C.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Neuroinflammatory signaling pathways in the central nervous system are of current interest as potential pharmacotherapy targets for alcohol dependence. In this study, we examined the ability of ibudilast, a non‐selective phosphodiesterase inhibitor, to reduce alcohol drinking and relapse in alcohol‐preferring P rats, high‐alcohol drinking HAD1 rats, and in mice made dependent on alcohol through cycles of alcohol vapor exposure. When administered twice daily, ibudilast reduced alcohol drinking in rats by approximately 50% and reduced drinking by alcohol‐dependent mice at doses which had no effect in non‐dependent mice. These findings support the viability of ibudilast as a possible treatment for alcohol dependence. In this study, we examined the ability of ibudilast, a non‐selective phosphodiesterase inhibitor, to reduce alcohol drinking and relapse in alcohol‐preferring P rats, high‐alcohol drinking HAD1 rats, and in mice made dependent on alcohol through cycles of alcohol vapor exposure. When administered twice daily, ibudilast reduced alcohol drinking in rats by approximately 50% and reduced drinking by alcohol dependent mice at doses which had no effect in non‐dependent mice.
ISSN:1355-6215
1369-1600
1369-1600
DOI:10.1111/adb.12106