Li Yuanrong, Wang Lixin, Sun Youhui, Wang Xuyi
Department of Psychiatry, and National Clinical Research Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Department of Psychiatry, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui, China.
Addict Biol. 2025 Sep;30(9):e70084. doi: 10.1111/adb.70084.
Valproate may hold promise as a treatment for addiction. However, there are limited studies examining the effects of magnesium valproate (VPA-Mg) on methamphetamine (MA) addiction, and the relevant mechanisms have not been thoroughly discussed. This study aims to explore the potential therapeutic effects of VPA-Mg on MA addiction and to investigate its possible mechanisms. The effects of VPA-Mg on MA addiction were investigated using conditioned place preference (CPP) and behavioural sensitisation models in rats. VPA-Mg was administered during CPP formation and extinction phases to evaluate its effects on MA-induced CPP formation and reinstatement. Behavioural sensitisation assessed the impact of VPA-Mg during sensitisation induction and expression phases, with spontaneous activity and MA dosing optimised beforehand. Furthermore, western blotting was performed on brain regions including the prefrontal cortex (PFC), hippocampus (Hip), nucleus accumbens (NAc) and ventral tegmental area (VTA) to measure glycogen synthase kinase 3 beta (GSK-3β) and dopamine transporter (DAT) protein levels. VPA-Mg did not exhibit a significant impact on MA-induced CPP formation. VPA-Mg significantly reduced the establishment and expression of MA-induced behavioural sensitisation (p < 0.01). Pre-treatment with VPA-Mg for 3 days before the expression period also inhibited sensitisation (p < 0.05). In addition, the ratio of p-GSK-3β to t-GSK-3β in the PFC, Hip and VTA of rats with behavioural sensitisation significantly decreased, and the expression of DAT decreased significantly (p < 0.01). VPA-Mg can reverse the increase in GSK-3β activity in the Hip and the decrease in DAT in the PFC and Hip caused by repeated MA use (p < 0.05). VPA-Mg exhibits anti-addictive effects on MA dependence and relapse prevention. GSK-3β activation and DAT downregulation in addiction-related brain regions (PFC, Hip, VTA) are closely linked to MA addiction, suggesting potential therapeutic targets. VPA-Mg may exert its effects by modulating these pathways, particularly in the PFC and Hip.
丙戊酸盐可能有望成为一种成瘾治疗方法。然而,研究镁丙戊酸盐(VPA-Mg)对甲基苯丙胺(MA)成瘾影响的研究有限,且相关机制尚未得到充分探讨。本研究旨在探索VPA-Mg对MA成瘾的潜在治疗作用,并研究其可能的机制。使用条件性位置偏爱(CPP)和行为敏化模型在大鼠中研究VPA-Mg对MA成瘾的影响。在CPP形成和消退阶段给予VPA-Mg,以评估其对MA诱导的CPP形成和恢复的影响。行为敏化评估VPA-Mg在敏化诱导和表达阶段的影响,预先优化自发活动和MA给药剂量。此外,对包括前额叶皮质(PFC)、海马体(Hip)、伏隔核(NAc)和腹侧被盖区(VTA)在内的脑区进行蛋白质免疫印迹法,以测量糖原合酶激酶3β(GSK-3β)和多巴胺转运体(DAT)蛋白水平。VPA-Mg对MA诱导的CPP形成没有显著影响。VPA-Mg显著降低了MA诱导的行为敏化的建立和表达(p < 0.01)。在表达期前用VPA-Mg预处理3天也抑制了敏化(p < 0.05)。此外,行为敏化大鼠的PFC、Hip和VTA中p-GSK-3β与t-GSK-3β的比值显著降低,DAT的表达显著降低(p < 0.01)。VPA-Mg可以逆转反复使用MA导致的Hip中GSK-3β活性增加以及PFC和Hip中DAT减少的情况(p < 0.05)。VPA-Mg对MA依赖和预防复发具有抗成瘾作用。成瘾相关脑区(PFC、Hip、VTA)中GSK-3β激活和DAT下调与MA成瘾密切相关,提示潜在的治疗靶点。VPA-Mg可能通过调节这些途径发挥作用,尤其是在PFC和Hip中。