Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol preferring (P) rats

dc.contributor.authorDing, Zheng-Ming
dc.contributor.authorRodd, Zachary A.
dc.contributor.authorEngleman, Eric A.
dc.contributor.authorBailey, Jason A.
dc.contributor.authorLahiri, Debomoy K.
dc.contributor.authorMcBride, William J.
dc.contributor.departmentPsychiatry, School of Medicine
dc.date.accessioned2025-05-30T12:14:03Z
dc.date.available2025-05-30T12:14:03Z
dc.date.issued2013
dc.description.abstractThe present study determined the effects of voluntary ethanol drinking and deprivation on basal extracellular glutamate concentrations and clearance in the mesolimbic system and tested the hypothesis that chronic ethanol drinking would persistently increase basal glutamate neurotransmission. Three groups of alcohol-preferring (P) rats were used: 'water group (WG),' 'ethanol maintenance group (MG; 24-hour free choice water versus 15% ethanol)' and 'ethanol deprivation group (DG; 2 weeks of deprivation).' Quantitative microdialysis and Western blots were conducted to measure basal extracellular glutamate concentrations, clearance and proteins associated with glutamate clearance. Chronic alcohol drinking produced a 70-100% increase of basal extracellular glutamate concentrations in the posterior ventral tegmental area (4.0 versus 7.0 μM) and nucleus accumbens shell (3.0 versus 6.0 μM). Glutamate clearances were reduced by 30-40% in both regions of MG rats compared with WG rats. In addition, Western blots revealed a 40-45% decrease of excitatory amino transporter 1 (EAAT1) protein, but no significant changes in the levels of EAAT2 or cystine-glutamate antiporter in these regions of MG versus WG rats. The enhanced glutamate concentrations returned to control levels, accompanied by a recovery of glutamate clearance following deprivation. These results indicated that chronic alcohol drinking enhanced extracellular glutamate concentrations in the mesolimbic system, as a result, in part, of reduced clearance, suggesting that enhanced glutamate neurotransmission may contribute to the maintenance of alcohol drinking. However, because the increased glutamate levels returned to normal after deprivation, elevated glutamate neurotransmission may not contribute to the initiation of relapse drinking.
dc.eprint.versionAuthor's manuscript
dc.identifier.citationDing ZM, Rodd ZA, Engleman EA, Bailey JA, Lahiri DK, McBride WJ. Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol-preferring (P) rats. Addict Biol. 2013;18(2):297-306. doi:10.1111/adb.12018
dc.identifier.urihttps://hdl.handle.net/1805/48492
dc.language.isoen_US
dc.publisherWiley
dc.relation.isversionof10.1111/adb.12018
dc.relation.journalAddiction Biology
dc.rightsPublisher Policy
dc.sourcePMC
dc.subjectAlcohol drinking
dc.subjectAlcohol deprivation
dc.subjectAlcohol preferring (P) rats
dc.subjectGlutamate neurotransmission
dc.subjectGlutamate transporter
dc.subjectNucleus accumbens
dc.subjectVentral tegmental area
dc.titleAlcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol preferring (P) rats
dc.typeArticle
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