Reduced effect of NMDA glutamate receptor antagonist on ethanol-induced ataxia and striatal glutamate levels in mice lacking ENT1

Hyung Wook Nam, Moonnoh R. Lee, David J. Hinton, Doo Sup Choi

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Alcohol-sensitive type 1 equilibrative nucleotide transporter (ENT1) is known to regulate glutamate signaling in the striatum as well as ethanol intoxication. However, it was unclear whether altered extracellular glutamate levels in ENT1-/- mice contribute to ethanol-induced behavioral changes. Here we report that altered glutamate signaling in ENT1-/- mice is implicated in the ethanol-induced locomotion and ataxia by NMDA receptor antagonist, CGP37849. ENT1-/- mice appear less intoxicated following sequential treatment with CGP37849 and ethanol, compared to ENT1+/+ littermates on the rotarod. These results indicate that inhibiting NMDA glutamate receptors is critical to regulate the response and susceptibility of alcohol related behaviors. Interestingly, a microdialysis experiment showed that the ventral striatum of ENT1-/- mice is less sensitive to the glutamate-reducing effect of the NMDA receptor antagonist compared to the dorsal striatum. Our findings suggest that differential glutamate neurotransmission in the striatum regulates ethanol intoxication.

Original languageEnglish (US)
Pages (from-to)277-281
Number of pages5
JournalNeuroscience Letters
Volume479
Issue number3
DOIs
StatePublished - Aug 1 2010

Keywords

  • Alcoholism
  • Ataxia
  • CGP37849
  • Caudate-putamen
  • ENT1
  • Glutamate neurotransmission
  • Microdialysis
  • Nucleus accumbens

ASJC Scopus subject areas

  • Neuroscience(all)

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