Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol-preferring (P) rats.
Alcohol drinking and deprivation alter basal extracellular glutamate concentrations and clearance in the mesolimbic system of alcohol-preferring (P) rats.
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DOI：
10.1111/adb.12018
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发表时间：
2013-03
影响因子：
3.4
通讯作者：
McBride WJ
中科院分区：
文献类型：
--
作者：
Ding ZM;Rodd ZA;Engleman EA;Bailey JA;Lahiri DK;McBride WJ
The 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-hr free choice water vs 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 vs 7.0 μM) and nucleus accumbens shell (3.0 vs 6.0 μM). Glutamate clearances were reduced by 30-40% in both regions of MG rats compared to 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 vs 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, since the increased glutamate levels returned to normal after deprivation, elevated glutamate neurotransmission may not contribute to the initiation of relapse drinking.
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影响因子：
4.7
作者：
Karlsson RM;Adermark L;Molander A;Perreau-Lenz S;Singley E;Solomon M;Holmes A;Tanaka K;Lovinger DM;Spanagel R;Heilig M
通讯作者：
Heilig M
DOI：
10.1111/j.1530-0277.2011.01665.x
发表时间：
2012-04-01
影响因子：
3.2
作者：
Ding, Zheng-Ming;Engleman, Eric A.;McBride, William J.
通讯作者：
McBride, William J.
DOI：
10.1111/j.1530-0277.2009.00985.x
发表时间：
2009-09-01
影响因子：
3.2
作者：
Ding, Zheng-Ming;Rodd, Zachary A.;McBride, William J.
通讯作者：
McBride, William J.
DOI：
10.1097/01.alc.0000187594.92476.07
发表时间：
2005-11-01
影响因子：
3.2
作者：
Kim, JH;Do, SH;Zuo, ZY
通讯作者：
Zuo, ZY
影响因子：
1.7
作者：
Lee, Eun;Jang, Dong-Pyo;Namkoong, Kee
通讯作者：
Namkoong, Kee