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Increased synaptic excitation and abnormal dendritic structure of prefrontal cortex layer V pyramidal neurons following prolonged binge-like consumption of ethanol

机译:长时间暴饮暴食乙醇后前额叶皮层V锥体神经元的突触兴奋和树突结构异常

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摘要

Long-term alcohol use causes a multitude of neurochemical changes in cortical regions which facilitate the transition to dependence. Therefore, we used a model of long-term, binge-like ethanol consumption in rats to determine the effects on morphology and synaptic physiology of (mPFC) layer V neurons. Following 10 weeks of ethanol consumption, we recorded synaptic currents from mPFC neurons and used Neurobiotin filling to analyse their morphology. We then compared this data to measurements obtained from age-matched water drinking control rats. We found that long-term ethanol consumption caused a significant increase in total dendrite arbor length of mPFC layer V neurons. Dendritic restructuring was primarily observed in basal dendrite arbors, with mPFC neurons from long-term ethanol drinking animals having significantly larger and more complex basal arbors compared to controls. These changes were accompanied by significantly increased total spine densities and spontaneous post-synaptic excitatory current frequency, suggesting that long-term binge-like ethanol consumption enhances basal excitatory synaptic transmission in mPFC layer V neurons. Our results provide insights into the morphological and functional changes in mPFC layer V pyramidal neuronal physiology following prolonged exposure to ethanol and support changes in mPFC activity during the development of alcohol dependence.
机译:长期饮酒会导致皮质区域发生多种神经化学变化,从而促进向依赖的转变。因此,我们使用了大鼠长期暴饮样乙醇消耗的模型来确定对(mPFC)V层神经元的形态和突触生理的影响。饮用乙醇10周后,我们记录了来自mPFC神经元的突触电流,并使用Neurobiotin填充物分析了它们的形态。然后,我们将该数据与从年龄匹配的饮水对照大鼠获得的测量值进行了比较。我们发现长期的乙醇消耗导致mPFC层V神经元的总枝状乔木长度显着增加。树突重构主要在基底树突状柄中观察到,与对照相比,长期饮酒动物的mPFC神经元具有明显更大,更复杂的基底树状柄。这些变化伴随着总脊柱密度的显着增加和突触后自发的自发性电流频率的增加,表明长期暴饮暴食的乙醇消耗增强了mPFC V层神经元的基础兴奋性突触传递。我们的结果提供了对长时间暴露于乙醇后mPFC V层锥体神经元生理学形态和功能变化的见解,并支持了在酒精依赖发展过程中mPFC活性的变化。

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