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

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 medial prefrontal cortex (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.