V. V. Zakusov Research Institute of Pharmacology, Moscow, Russia.
Bull Exp Biol Med. 2020 Nov;170(1):30-34. doi: 10.1007/s10517-020-04998-0. Epub 2020 Nov 22.
Activity of compound GSB-106, a low-molecular mimetic of loop 4 of the brain neurotrophic factor (BDNF), was studied in experimental morphine withdrawal syndrome simulated in outbred rats. Single and subchronic (5 intraperitoneal injections) administration of GSB-106 in a dose of 0.1 mg/kg significantly reduced the total index of morphine withdrawal syndrome by 55.2 and 45.6%, respectively. GSB-106 reduced the severity of some behavioral signs (piloerection, gnashing of teeth, wet-dog shaking, and runaway attempts), but had no effect on mechanical allodynia formed in the rats with dependence. Subchronic treatment with GSB-106 prevented the increase in the content of ΔFosB (product of early response gene) in the striatum induced by morphine withdrawal. The results confirmed the concept on the involvement of neurotrophins, specifically BDNF and its analogs, in the mechanisms associated with the formation of opiate dependence.
实验性吗啡戒断综合征在杂种大鼠中模拟，研究了脑源性神经营养因子（BDNF）环 4 小分子模拟物 GSB-106 的活性。GSB-106 单次和亚慢性（5 次腹腔注射）给药 0.1mg/kg 剂量可分别使吗啡戒断综合征总指数降低 55.2%和 45.6%。GSB-106 降低了一些行为征象的严重程度（竖毛、咬牙切齿、湿狗抖动和失控尝试），但对依赖大鼠形成的机械性痛觉过敏没有影响。GSB-106 的亚慢性治疗可预防吗啡戒断引起的纹状体中 ΔFosB（早期反应基因产物）含量的增加。结果证实了神经营养因子，特别是 BDNF 及其类似物参与与阿片类药物依赖形成相关机制的概念。
