Tolerance to ethanol intoxication after chronic ethanol: role of GluN2A and PSD-95.
| Autor: | Daut RA; Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcoholism and Alcohol Abuse, NIH, Bethesda, MD, USA., Busch EF, Ihne J, Fisher D, Mishina M, Grant SG, Camp M, Holmes A |
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| Jazyk: | angličtina |
| Zdroj: | Addiction biology [Addict Biol] 2015 Mar; Vol. 20 (2), pp. 259-62. Date of Electronic Publication: 2014 Jan 07. |
| DOI: | 10.1111/adb.12110 |
| Abstrakt: | 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. (© 2014 Society for the Study of Addiction.) |
| Databáze: | MEDLINE |
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