Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala

被引:28
作者
Laeck, A. K. [1 ]
Christian, D. T. [1 ,2 ]
Diaz, M. R. [3 ]
McCool, B. A. [1 ,2 ,3 ]
机构
[1] Wake Forest Univ, Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27157 USA
[2] Wake Forest Univ, Sch Med, Alcohol Training Program, Winston Salem, NC 27157 USA
[3] Wake Forest Univ, Sch Med, Neurosci Training Program, Winston Salem, NC 27157 USA
关键词
Basolateral amygdala; Electrophysiology; Kainate; Anxiety; Withdrawal; LONG-TERM POTENTIATION; ANXIETY-LIKE BEHAVIOR; PHASEOLUS-VULGARIS-LEUKOAGGLUTININ; IN-VITRO; GLUTAMATERGIC SYNAPSES; ENTORHINAL CORTEX; DEPENDENT RATS; DENTATE GYRUS; NEURONS; HIPPOCAMPUS;
D O I
10.1016/j.alcohol.2008.11.002
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
Withdrawal (WD) anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is extensive, long-lasting, and develops well after the obvious physical symptoms of acute WD. The neurobiological mechanisms underlying this prolonged WD-induced anxiety are not well understood. The basolateral amygdala (BLA) is a major emotional center in the brain and regulates the expression of anxiety. New evidence suggests that increased glutamatergic function in the BLA may contribute to WD-related anxiety following chronic ethanol exposure. Recent evidence also suggests that kainate-type ionotropic glutamate receptors are inhibited by intoxicating concentrations of acute ethanol. This acute sensitivity suggests potential (KA-R) contributions by these receptors to the increased glutamatergic function seen during chronic exposure. Therefore, we examined the effect of chronic intermittent ethanol (CIE) and WD on KA-R-mediated synaptic transmission in the BLA of Sprague-Dawley rats. Our study showed that CIE, but not WD, increased synaptic responses mediated by KA-Rs. Interestingly, both CIE and WD occluded KA-R-mediated synaptic plasticity. Finally, we found that BLA field excitatory postsynaptic potential responses were increased during CIE and WD via a mechanism that is independent of glutamate release from presynaptic terminals. Taken together, these data suggest that KA-Rs might contribute to postsynaptic increases in glutamatergic synaptic transmission during CIE and that the mechanisms responsible for the expression of KA-R-dependent synaptic plasticity might be engaged by chronic ethanol exposure and WD. (C) 2009 Elsevier Inc. All rights reserved.
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页码:25 / 33
页数:9
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