Janner Dieniffer Espinosa, Gomes Nathalie Savedra, Poetini Márcia Rósula, Poleto Kétnne Hanna, Musachio Elize Aparecida Santos, de Almeida Francielli Polet, de Matos Amador Elen Caroline, Reginaldo Jocemara Corrêa, Ramborger Bruna Piaia, Roehrs Rafael, Prigol Marina, Guerra Gustavo Petri
Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas - LaftamBio, Universidade Federal do Pampa, Campus Itaqui, 97650-000, Itaqui, RS, Brazil; Programa de Pós-Graduação em Bioquímica, Universidade Federal do Pampa, Campus Uruguaiana, 97508-000, Uruguaiana, RS, Brazil.
Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas - LaftamBio, Universidade Federal do Pampa, Campus Itaqui, 97650-000, Itaqui, RS, Brazil.
Neurotoxicology. 2021 Jul;85:79-89. doi: 10.1016/j.neuro.2021.05.006. Epub 2021 May 14.
Neurodevelopmental disorders, such as Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD) are responsible for behavioral deficits in children. Imidacloprid is a nicotinic acetylcholine receptor agonist, capable of causing behavioral changes in Drosophila melanogaster, similar to the ADHD-like phenotypes. We assess whether behavioral damage induced by imidacloprid exposure in Drosophila melanogaster is associated with neurochemical changes and whether these changes are similar to those observed in neurodevelopmental disorders such as ASD and ADHD. The fruit flies were divided into four groups, exposed to either a standard diet (control) or a diet containing imidacloprid (200, 400 or 600 ρM) and allowed to mate for 7 days. After hatching, the progeny was subjected to in vivo and ex vivo tests. The ones exposed to imidacloprid showed an increase in hyperactivity, aggressiveness, anxiety and repetitive movements, as well as, a decrease in social interaction. Furthermore, exposure to imidacloprid decreased dopamine levels, cell viability and increased oxidative stress in the flies' progeny. These results demonstrated that the behavioral damage induced by imidacloprid exposure involves a reduction in dopamine levels and oxidative stress and that these neurochemical changes are in line with the events that occur in ASD and ADHD-like phenotypes in other models.
神经发育障碍，如自闭症谱系障碍（ASD）和注意力缺陷多动障碍（ADHD），会导致儿童出现行为缺陷。吡虫啉是一种烟碱型乙酰胆碱受体激动剂，能够在黑腹果蝇中引起行为变化，类似于ADHD样表型。我们评估了吡虫啉暴露在黑腹果蝇中诱导的行为损伤是否与神经化学变化相关，以及这些变化是否与在诸如ASD和ADHD等神经发育障碍中观察到的变化相似。将果蝇分为四组，分别喂食标准饮食（对照组）或含有吡虫啉（200、400或600 μM）的饮食，并使其交配7天。孵化后，对后代进行体内和体外测试。暴露于吡虫啉的果蝇表现出多动、攻击性、焦虑和重复动作增加，以及社交互动减少。此外，暴露于吡虫啉会降低果蝇后代的多巴胺水平、细胞活力并增加氧化应激。这些结果表明，吡虫啉暴露诱导的行为损伤涉及多巴胺水平降低和氧化应激，并且这些神经化学变化与其他模型中ASD和ADHD样表型中发生的事件一致。
