Abstract
Sleep loss is associated with a potential risk of using drugs such as cocaine, methamphetamines, and alcohol. Recently, our group showed that chronic sleep restriction (CSR) for 7 days/4 h induces a significant increase in ethanol intake and delta FosB immunoreactivity in the rat's prefrontal cortex. However, whether CSR promotes changes in structural plasticity that explain ethanol consumption is unknown. Therefore, the present study aimed to determine if CSR induces changes in the dendritic length, branching of the dendritic tree, and spine morphology of the pyramidal neurons from the prelimbic cortex and whether these structural changes are associated with ethanol consumption. For this purpose, adult male Wistar rats were divided into four experimental groups: control, CSR for 7 days/4 h daily, CSR + ethanol exposure, and ethanol exposure. The two-bottle free-choice paradigm was used to measure ethanol intake, and the gentle handling method was used for CSR. At the end of the experiment, the rats were euthanized, and their brains were dissected and processed by Golgi-Cox staining. Sholl analysis was used to characterize structural plasticity. Results show that CSR induced an increase in the ethanol index preference. In addition, ethanol intake and ethanol + CSR increased the total dendritic length, dendritic tree branching, and mushroom spines in prelimbic cortex neurons. In conclusion, changes in structural plasticity associated with CSR and continuous access to ethanol may translate into neuroadaptive changes that favor drug preference and subsequently reinforce addictive behavior.