Lipaus Ingryd Fortes Souza, Gomes Elisa Fraga, Martins Cleciane Waldetário, E Silva Cristina Martins, Pires Rita Gomes Wanderley, Malgarin Fernanda, Schuck Patrícia Fernanda, Palacios Ester Miyuki Nakamura, de Melo Rodrigues Lívia Carla
Laboratory of Neurotoxicology and Psychopharmacology, Program of Post-Graduation in Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil; Laboratory of Cognitive Sciences and Neuropsychopharmacology, Program of Post-Graduation in Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil.
Laboratory of Molecular and Behavioral Neurobiology, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil.
Behav Brain Res. 2019 Feb 1;359:910-917. doi: 10.1016/j.bbr.2018.06.020. Epub 2018 Jun 20.
Crack cocaine is a highly toxic drug with great potential to induce addiction. It produces more intense effects than cocaine powder, with its use having grown worldwide. However, few studies have focused on the cognitive and biochemical consequences that result from crack cocaine inhalation. This study examined the effects of direct crack cocaine inhalation on spatial working memory and brain oxidative stress parameters in rats. Male adult Wistar rats, well-trained in an eight-arm radial maze (8-RM), underwent five sessions of crack cocaine inhalation (crack cocaine group) once a day or inhalation simulation (sham group), being tested in 1-h delayed tasks 24 h after the last inhalation. An additional inhalation session was carried out the following day, with the prefrontal cortex, hippocampus and striatum being removed five minutes afterwards in order to assess oxidative damage such as lipid peroxidation, thiobarbituric acid-reactive species (TBARS) levels, and advanced oxidation protein products (AOPP), as well as the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Animals from the crack cocaine group showed more errors (p < 0.01) in the 1-h post-delay performance in the 8-RM when compared to the sham group. The crack cocaine group showed decreased (p < 0.05) lipid peroxidation in the hippocampus and increased (p < 0.001) levels of AOPP and SOD activity (p < 0.05) in the striatum when compared to the sham group. Therefore, the repeated inhalation of crack cocaine impaired long-term spatial working memory and elicited oxidative stress in the hippocampus and striatum of rats.
快克可卡因是一种剧毒药物，极易使人上瘾。它比可卡因粉末产生的效果更强烈，在全球范围内其使用量不断增加。然而，很少有研究关注吸入快克可卡因所导致的认知和生化后果。本研究检测了直接吸入快克可卡因对大鼠空间工作记忆和脑氧化应激参数的影响。在八臂放射状迷宫（8-RM）中接受过良好训练的成年雄性Wistar大鼠，每天接受一次共五次的快克可卡因吸入（快克可卡因组）或吸入模拟（假手术组），在最后一次吸入后24小时进行1小时延迟任务测试。次日再进行一次吸入，随后5分钟取出前额叶皮质、海马体和纹状体，以评估氧化损伤，如脂质过氧化、硫代巴比妥酸反应性物质（TBARS）水平和晚期氧化蛋白产物（AOPP），以及抗氧化酶如超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）的活性。与假手术组相比，快克可卡因组的大鼠在8-RM延迟1小时后的表现中出现了更多错误（p<0.01）。与假手术组相比，快克可卡因组海马体中的脂质过氧化水平降低（p<0.05），纹状体中的AOPP水平升高（p<0.001），SOD活性增强（p<0.05）。因此，反复吸入快克可卡因会损害大鼠的长期空间工作记忆，并在其海马体和纹状体中引发氧化应激。
