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首页> 外文期刊>Alcohol >Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.
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Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.

机译：慢性乙醇和戒断对大鼠基底外侧杏仁核中的海藻酸盐受体介导的兴奋性神经传递的影响。

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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.
机译：戒酒（WD）焦虑是导致酗酒者持续酗酒的重要因素。这种焦虑是广泛的，持久的，并且在急性WD的明显身体症状出现后会迅速发展。这种长期的WD引起的焦虑的神经生物学机制尚未得到很好的理解。基底外侧杏仁核（BLA）是大脑中的主要情感中心，它调节焦虑的表达。新证据表明，慢性乙醇暴露后，BLA中谷氨酸能功能的增强可能导致与WD相关的焦虑。最近的证据还表明，中毒浓度的急性乙醇可抑制海藻酸盐型离子型谷氨酸受体。这种急性敏感性表明，这些受体可能对慢性暴露期间增加的谷氨酸能功能产生潜在的（KA-R）贡献。因此，我们检查了慢性间歇性乙醇（CIE）和WD对Sprague-Dawley大鼠BLA中KA-R介导的突触传递的影响。我们的研究表明，CIE而非WD可以增加由KA-R介导的突触反应。有趣的是，CIE和WD都堵塞了KA-R介导的突触可塑性。最后，我们发现通过独立于突触前末端谷氨酸释放的机制，在CIE和WD期间BLA场兴奋性突触后电位反应增加。综上所述，这些数据表明，KA-Rs可能有助于CIE期间谷氨酸能突触传递的突触后增加，并且慢性乙醇暴露和WD可能参与了负责表达KA-R依赖性突触可塑性的机制。

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