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Electroconvulsive seizures protect against methamphetamine-induced inhibition of neurogenesis in the rat hippocampus
NeuroToxicology ( IF 3.4 ) Pub Date : 2021-08-18 , DOI: 10.1016/j.neuro.2021.08.008
Rubén García-Cabrerizo 1 , Cristian Bis-Humbert 1 , M Julia García-Fuster 1
Affiliation  

Following methamphetamine consumption and during abstinence many behavioral consequences emerge (i.e., cognitive deficits, ongoing episodes of psychosis, depression, severe cravings, brain neurotoxicity), which are likely linked to propensity to relapse. In this line of thought, we recently showed that binge methamphetamine administration enhanced negative affect and voluntary drug consumption in rats, while it induced persistent neurotoxic effects (i.e., impaired hippocampal neurogenesis), effects that emerged long after drug removal. To date, no pharmacological strategies have been proven to be effective for the treatment of methamphetamine toxicity. A few studies have evaluated the impact of combining methamphetamine pretreatment with electroconvulsive seizures (ECS) post-treatment, an alternative non-pharmacological option used in psychiatry for resistant depression that offers a safe and really potent therapeutic response. Against this background, the present study aimed at testing whether repeated ECS treatment could ameliorate some of the long-term neurotoxicity effects induced by adolescent methamphetamine exposure in rats and emerging after drug removal. At the behavioral level, the main results showed that methamphetamine administration did not alter negative affect immediate during adolescence or later on in adulthood. Interestingly, repeated ECS improved the negative impact of methamphetamine administration on reducing hippocampal neurogenesis, demonstrating that ECS can attenuate certain degree of methamphetamine-induced neurotoxicity in rats, and suggesting ECS as a good therapeutical candidate that deserves further studies.



中文翻译:

电惊厥发作可防止甲基苯丙胺诱导的大鼠海马神经发生抑制

甲基苯丙胺消费后和禁欲期间会出现许多行为后果(即认知缺陷、持续的精神病发作、抑郁、严重的渴望、脑神经毒性),这可能与复发倾向有关。在这一思路中,我们最近表明,狂饮甲基苯丙胺会增强大鼠的负面影响和自愿药物消耗,同时它会引起持续的神经毒性作用(即受损的海马神经发生),这些作用在药物去除后很久就出现了。迄今为止,没有药理学策略被证明可有效治疗甲基苯丙胺毒性。一些研究评估了甲基苯丙胺预处理与电惊厥发作 (ECS) 后处理相结合的影响,精神病学中用于抵抗性抑郁症的另一种非药物选择,可提供安全且真正有效的治疗反应。在此背景下,本研究旨在测试反复 ECS 治疗是否可以改善因青少年甲基苯丙胺暴露在大鼠中以及在药物去除后出现的一些长期神经毒性作用。在行为层面,主要结果表明甲基苯丙胺给药不会立即改变青春期或成年后期的负面影响。有趣的是,重复 ECS 改善了甲基苯丙胺给药对减少海马神经发生的负面影响,表明 ECS 可以减轻甲基苯丙胺诱导的大鼠神经毒性的一定程度,

更新日期:2021-08-21
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