Departamento de Biociências, Universidade Federal de São Paulo (UNIFESP), Santos, São Paulo, Brazil.
Exp Brain Res. 2022 Dec;240(12):3107-3140. doi: 10.1007/s00221-022-06479-4. Epub 2022 Oct 20.
This systematic review (SR) was aimed at answering two questions: (1) how sex and ovarian hormones alter behavior associated with cocaine use; (2) which possible neurobiological mechanisms explain behavioral differences. Three different researchers conducted a search in PUBMED for all kinds of articles published between the years of 1991 to 2021 on the theme "reproductive cycle and cocaine", "estrous cycle and cocaine", "menstrual cycle and cocaine", "fluctuation of ovarian hormones and cocaine", "estrogen and cocaine" and "progesterone and cocaine". Sixty original studies were identified and subdivided into experimental rodent studies and clinical trials. Experimental studies were characterized by author/year, species/strain, sex/number, age/weight, dose/route/time of administration, hormonal assessment, or administration. Clinical trials were characterized by author/year, sex/number, age, exclusion criterion, dose/route of administration/time of cocaine, and hormonal assessment. Results gathered showed that rodent females develop increased consumption, seeking behavior, craving, relapse, locomotion, increases in stress and anxiety, among other behavioral alterations during peaks of estrogen. These observations are related to the direct effects played by ovarian hormones (in particularly estradiol), in dopamine, but also in serotonin neurons, and in brain regions such as the tegmental area, the nucleus accumbens, the hypothalamus, the amygdala and the prefrontal cortex. Increased sensitization to cocaine presented by high estradiol females was linked to the activation of a CBR1-mediated mechanism and GABA-A-dependent suppression of inhibitory synaptic activity of the prelimbic prefrontal cortex. Estradiol facilitation of cocaine-increased locomotion and self-administration was shown to require the release of glutamate and the activation of metabotropic glutamate receptors subtype 5. Clinical studies also tend to point to a stimulatory effect of estradiol on cocaine sensitization and a neuroprotective effect of progesterone. In conclusion, the results of the present review indicate a need for further preclinical and clinical trials and neurobiological studies to better understand the relationship between sex and ovarian hormones on cocaine sensitization.
本系统评价(SR)旨在回答两个问题:(1)性别和卵巢激素如何改变与可卡因使用相关的行为;(2)哪些可能的神经生物学机制解释了行为差异。三位不同的研究人员在 PUBMED 中搜索了 1991 年至 2021 年期间发表的所有主题为“生殖周期和可卡因”、“发情周期和可卡因”、“月经周期和可卡因”、“卵巢激素波动和可卡因”、“雌激素和可卡因”和“孕激素和可卡因”的文章。确定了 60 篇原始研究,并分为实验性啮齿动物研究和临床试验。实验研究的特征是作者/年份、物种/品系、性别/数量、年龄/体重、剂量/给药途径/时间、激素评估或给药。临床试验的特征是作者/年份、性别/数量、年龄、排除标准、可卡因的剂量/给药途径/时间和激素评估。收集的结果表明,在雌激素高峰期,雌性啮齿动物会出现行为改变,包括消费增加、寻求行为、渴望、复发、运动增加、压力和焦虑增加等。这些观察结果与卵巢激素(特别是雌二醇)、多巴胺、5-羟色胺神经元以及中脑腹侧被盖区、伏隔核、下丘脑、杏仁核和前额叶皮质等脑区直接作用有关。高雌二醇雌性对可卡因的敏感性增加与 CBR1 介导的机制的激活以及前扣带回皮层抑制性突触活动的 GABA-A 依赖性抑制有关。雌二醇促进可卡因增加的运动和自我给药需要谷氨酸的释放和代谢型谷氨酸受体亚型 5 的激活。临床研究也倾向于表明雌二醇对可卡因敏化有刺激作用,孕激素有神经保护作用。总之,本综述的结果表明,需要进一步进行临床前和临床试验以及神经生物学研究,以更好地理解性别和卵巢激素对可卡因敏化的关系。