Bravo-González Fernando, Acosta-Hernández Mario Eduardo, Tendilla-Beltrán Hiram, Flores Gonzalo, García-García Fabio
Graduate Program in Health Sciences. Institute of Health Sciences, Veracruzana University, Xalapa, VER, 91190, Mexico.
Department of Biomedicine, Health Sciences Institute, Veracruzana University, Xalapa, VER, 91190, Mexico.
Neurobiol Sleep Circadian Rhythms. 2025 May 14;18(Suppl):100126. doi: 10.1016/j.nbscr.2025.100126. eCollection 2025 May.
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.
睡眠不足与使用可卡因、甲基苯丙胺和酒精等药物的潜在风险有关。最近，我们的研究小组表明，连续7天每天4小时的慢性睡眠限制（CSR）会导致大鼠前额叶皮质中乙醇摄入量和δFosB免疫反应性显著增加。然而，CSR是否会促进解释乙醇消费的结构可塑性变化尚不清楚。因此，本研究旨在确定CSR是否会诱导前边缘皮质锥体细胞的树突长度、树突分支和棘形态发生变化，以及这些结构变化是否与乙醇消费有关。为此，将成年雄性Wistar大鼠分为四个实验组：对照组、每天进行7天/4小时的CSR组、CSR+乙醇暴露组和乙醇暴露组。采用双瓶自由选择范式测量乙醇摄入量，采用轻柔处理方法进行CSR。实验结束时，对大鼠实施安乐死，并解剖其大脑，用高尔基-考克斯染色法进行处理。采用Sholl分析来表征结构可塑性。结果表明，CSR诱导乙醇指数偏好增加。此外，乙醇摄入量以及乙醇+CSR增加了前边缘皮质神经元的总树突长度、树突分支和蘑菇状棘。总之，与CSR和持续接触乙醇相关的结构可塑性变化可能转化为有利于药物偏好并随后强化成瘾行为的神经适应性变化。
