![]() Prolonged alcohol use often involves repeated cycles of binge-like intake and abstinence, which produces adaptive changes in the brain that alter decision-making and impulsivity, and that sensitize behavioral responses to negative symptoms of withdrawal ( Koob and Volkow, 2010). Long-term alcohol use has significantly different effects on the brain compared with short-term exposure ( Koob and Volkow, 2010). 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. These changes were accompanied by significantly increased total spine densities and spontaneous postsynaptic excitatory current frequency, suggesting that long-term binge-like ethanol consumption enhances basal excitatory synaptic transmission in mPFC layer V pyramidal neurons. Dendritic restructuring was primarily observed in basal dendrite arbors, with mPFC neurons from animals engaged in long-term ethanol drinking having significantly larger and more complex basal arbors compared with controls. We found that long-term ethanol consumption caused a significant increase in total dendrite arbor length of mPFC layer V pyramidal neurons. We then compared these data to measurements obtained from age-matched, water-drinking control rats. Following 10 weeks of ethanol consumption, we recorded synaptic currents from mPFC neurons and used neurobiotin filling to analyze their morphology. Therefore, we used a model of long-term, binge-like ethanol consumption in rats to determine the effects on morphology and synaptic physiology of medial prefrontal cortex (mPFC) layer V pyramidal neurons. Long-term alcohol use causes a multitude of neurochemical changes in cortical regions that facilitate the transition to dependence.
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