Tolerance to ethanol intoxication after chronic ethanol: role of  G lu N 2 A  and  PSD ‐95 | Zendy

Daut Rachel A. | Zendy; Busch Erica F. | Zendy; Ihne Jessica | Zendy; Fisher Daniel | Zendy; Mishina Masayoshi | Zendy; Grant Seth G. N. | Zendy; Camp Marguerite | Zendy; Holmes Andrew | Zendy

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Tolerance to ethanol intoxication after chronic ethanol: role of G lu N 2 A and PSD ‐95

Author(s) -

Daut Rachel A.,

Busch Erica F.,

Ihne Jessica,

Fisher Daniel,

Mishina Masayoshi,

Grant Seth G. N.,

Camp Marguerite,

Holmes Andrew

Publication year - 2015

Publication title -

addiction biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.445

H-Index - 78

eISSN - 1369-1600

pISSN - 1355-6215

DOI - 10.1111/adb.12110

Subject(s) - ethanol , knockout mouse , receptor , alcohol , alcohol tolerance , gene knockout , nmda receptor , protein subunit , medicine , chemistry , endocrinology , gene , biochemistry

The neural and genetic factors underlying chronic tolerance to alcohol are currently unclear. The G lu N 2 A 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 C 57 BL /6 J , G lu N 2 A or PSD ‐95 knockout mice assayed 2–3 days later. However, significant tolerance to LORR was evident 1 day after CIE in C 57 BL /6 J and PSD ‐95 knockouts, but absent in G lu N 2 A knockouts. These data suggest a role for G lu N 2 A in tolerance, extending evidence that human G lu N 2 A gene variation is involved in alcohol dependence.

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