Effects of naltrexone and acamprosate on alcohol-induced NGFI-A expression in mouse brain

Jeanette Lindholm, Marc Guitart-Masip, Homa Hassankhali, Sara Landgren, Camille Nicoleau, Lydia Giménez-Llort, Lars Terenius, Sven Ove Ögren, Björn Johansson

Research output: Contribution to journalArticleResearchpeer-review

5 Citations (Scopus)

Abstract

In search for the substrate of naltrexone and acamprosate action on alcohol craving, we investigated the effects of ethanol alone and combined with naltrexone or acamprosate on expression of nerve growth factor-inducible clone A (NGFI-A; zif268). In Experiments 1 and 3, alcohol (2 g/kg) alone or in combination with naltrexone (15 mg/kg) or acamprosate (300 mg/kg) was injected intraperitoneally into mice. In Experiment 2, treatment was nor-BNI (0.5 mg/kg) to investigate whether the effect of naltrexone involved blockade of κ-opioid receptors. Both ethanol and naltrexone alone induced NGFI-A in the central amygdala, but not in several other areas; these effects were additive. However, acamprosate alone or in combination with ethanol had no effect on NGFI-A mRNA, while nor-BNI induced NGFI-A mRNA in the basolateral amygdala. The central amygdala appears to be an important target of both alcohol and naltrexone. Acamprosate may not share the site of action with naltrexone despite being used for the same therapeutic purpose. © 2008 Springer Science+Business Media, LLC.
Original languageEnglish
Pages (from-to)2062-2069
JournalNeurochemical Research
Volume33
Issue number10
DOIs
Publication statusPublished - 1 Jan 2008

Keywords

  • Acamprosate
  • Amygdala
  • Ethanol
  • Naltrexone
  • NGFI-A
  • zif268

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