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首页> 外文期刊>Neuropharmacology >Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol
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Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

机译：从慢性间歇性乙醇撤出后，丘脑向大鼠基底外侧杏仁核传入的谷氨酸能表现出增加的突触前谷氨酸功能

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Amygdala glutamatergic neurotransmission regulates withdrawal induced anxiety-like behaviors following chronic ethanol exposure. The lateral/basolateral amygdala receives multiple glutamatergic projections that contribute to overall amygdala function. Our lab has previously shown that rat cortical (external capsule) afferents express postsynaptic alterations during chronic intermittent ethanol exposure and withdrawal. However, thalamic (internal capsule) afferents also provide crucial glutamatergic input during behavioral conditioning, and they have not been studied in the context of chronic drug exposure. We report here that these thalamic inputs express altered presynaptic function during withdrawal from chronic ethanol exposure. This is characterized by enhanced release probability, as exemplified by altered paired-pulse ratios and decreased failure rates of unitary events, and increased concentrations of synaptic glutamate. Quantal analysis further implicates a withdrawal-dependent enhancement of the readily releasable pool of vesicles as a probable mechanism. These functional alterations are accompanied by increased expression of vesicle associated protein markers. These data demonstrate that chronic ethanol modulation of glutamate neurotransmission in the rat lateral/basolateral amygdala is afferent-specific. Further, presynaptic regulation of lateral/basolateral amygdala thalamic inputs by chronic ethanol may be a novel neurobiological mechanism contributing to the increased anxiety-like behaviors that characterize withdrawal.
机译：杏仁核的谷氨酸能神经传递调节慢性乙醇暴露后戒断引起的焦虑样行为。外侧/基底外侧杏仁核接收多个有助于整体杏仁核功能的谷氨酸能投射。我们的实验室先前已经证明，大鼠皮质（外部囊）传入神经在慢性间歇性乙醇暴露和戒断期间表达突触后改变。然而，丘脑（内囊）传入神经在行为调节过程中也提供了关键的谷氨酸能输入，尚未在慢性药物暴露的情况下对其进行研究。我们在这里报告说，这些丘脑输入表达从慢性乙醇暴露退出期间改变的突触前功能。其特征在于释放概率增加，例如改变的成对脉冲比率和单一事件失败率降低，以及突触谷氨酸浓度增加。量子分析进一步暗示了依赖释放的易于释放的囊泡池的增强是可能的机制。这些功能改变伴随着囊泡相关蛋白标志物表达的增加。这些数据证明大鼠外侧/基底外侧杏仁核中谷氨酸神经传递的慢性乙醇调节是传入特异性的。此外，慢性乙醇对侧/基底外侧杏仁核丘脑输入的突触前调节可能是一种新型的神经生物学机制，有助于增加以戒断为特征的焦虑样行为。

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