Addiction Biology Unit, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Alcohol Clin Exp Res. 2019 May;43(5):803-811. doi: 10.1111/acer.14014. Epub 2019 Apr 10.
Addiction has been conceptualized as a shift from controlled recreational use toward compulsive and habitual drug-taking behavior. Although the brain reward system is vital for alcohol reward and reinforcement, other neuronal circuits may be involved in controlling long-term alcohol-seeking and drug-taking behaviors. The aim of this study was to outline alcohol-induced neuroplasticity in defined cortical and striatal subregions, previously implicated in alcohol use disorder.
Male Wistar rats were allowed to voluntarily consume ethanol (EtOH) in an intermittent manner for 2 months, after which ex vivo electrophysiological recordings were performed and data compared with isolated water controls housed in parallel.
Field potential recordings revealed an increase in field excitatory postsynaptic potentials (fEPSPs) in the dorsomedial striatum (DMS) of rats consuming EtOH, while a depression of evoked potentials was detected in the dorsolateral striatum (DLS). Mean activity in cortical (medial prefrontal cortex, lateral orbitofrontal cortex [OFC]), and accumbal regions (nucleus accumbens [nAc] core/shell) was not significantly altered as compared to water-drinking controls, but a correlation between the amount of alcohol consumed and evoked potentials could be found in both dorsal striatal subregions, OFC, and nAc core. Removal of EtOH for 1 to 2 days was sufficient to restore neurotransmission in the DLS, while the increase in fEPSP amplitude sustained in the DMS.
These preclinical findings are in line with clinical observations indicating that alcohol produces neurophysiological transformations in dorsal striatal circuits, which in turn may lead to disruptions in decision-making processes that could further promote alcohol misuse.
成瘾被概念化为从受控的娱乐性使用向强迫性和习惯性药物使用行为的转变。尽管大脑奖励系统对酒精奖励和强化至关重要，但其他神经元回路可能参与控制长期的酒精寻求和药物使用行为。本研究的目的是概述先前与酒精使用障碍有关的特定皮质和纹状体亚区的酒精诱导的神经可塑性。
雄性 Wistar 大鼠被允许以间歇性方式自愿消耗乙醇（EtOH）2 个月，之后进行离体电生理记录，并将数据与并行饲养的孤立水对照进行比较。
场电位记录显示，消耗 EtOH 的大鼠背侧纹状体（DMS）中的场兴奋性突触后电位（fEPSP）增加，而背外侧纹状体（DLS）中的诱发电位被抑制。与饮水对照组相比，皮质（内侧前额叶皮层、外侧眶额皮层[OFC]）和伏隔核（伏隔核核心/壳）区域的平均活动没有明显改变，但可以在两个背侧纹状体亚区、OFC 和 nAc 核心中找到消耗的酒精量与诱发电位之间的相关性。EtOH 去除 1 至 2 天足以恢复 DLS 中的神经传递，而 DMS 中的 fEPSP 幅度增加持续存在。
这些临床前发现与临床观察一致，表明酒精在背侧纹状体回路中产生神经生理变化，这反过来可能导致决策过程中断，从而进一步促进酒精滥用。
