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Addict Biol. 2015 Mar;20(2):259-62. doi: 10.1111/adb.12110. Epub 2014 Jan 7.

Tolerance to ethanol intoxication after chronic ethanol: role of GluN2A and PSD-95.

Author information

1
Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcoholism and Alcohol Abuse, NIH, Bethesda, MD, USA.

Abstract

The neural and genetic factors underlying chronic tolerance to alcohol are currently unclear. The GluN2A N-methyl-D-aspartate receptors (NMDAR) subunit and the NMDAR-anchoring protein PSD-95 mediate acute alcohol intoxication and represent putative mechanisms mediating tolerance. We found that chronic intermittent ethanol exposure (CIE) did not produce tolerance [loss of righting reflex (LORR)] or withdrawal-anxiety in C57BL/6J, GluN2A or PSD-95 knockout mice assayed 2-3 days later. However, significant tolerance to LORR was evident 1 day after CIE in C57BL/6J and PSD-95 knockouts, but absent in GluN2A knockouts. These data suggest a role for GluN2A in tolerance, extending evidence that human GluN2A gene variation is involved in alcohol dependence.

KEYWORDS:

GluN2A and PSD-95; chronic ethanol; tolerance

PMID:
24397780
PMCID:
PMC4085154
DOI:
10.1111/adb.12110
[Indexed for MEDLINE]
Free PMC Article
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