Ashok Chetan, Rajasekaran Naveen Kumar, Jeyabalan Srikanth, Veeraraghavan Gayathri, Suresh Subalakshmi, Sugumar Ramya, Jabaris Sugin Lal, Subramaniyan Vetriselvan, Wong Ling Shing
Department of Pharmacology, Faculty of Pharmacy, Sri Ramachandra Institute of Higher Education and Research (DU), Chennai, Tamil Nadu 600 116, India.
Centre for Toxicology and Developmental Research (CEFTE), Sri Ramachandra Institute of Higher Education and Research (DU), Chennai, Tamil Nadu 600 116, India.
Toxicol Rep. 2025 Jul 12;15:102084. doi: 10.1016/j.toxrep.2025.102084. eCollection 2025 Dec.
Parkinson's disease (PD), a prevalent neurodegenerative disorder, is marked by dopaminergic neuron loss and motor impairments. This study aimed to establish and compare PD models in adult zebrafish using two neurotoxins, MPTP and rotenone, evaluating their impact on behaviour and histopathology. Zebrafish were exposed to MPTP via intraperitoneal injection at two different doses or to rotenone in water for 21 days. Behavioural assessments, including Novel Tank Diving Test, bradykinesia, and C-bend response, revealed progressive motor and anxiety-like impairments, with rotenone exhibiting stronger locomotor effects. Histopathological analyses confirmed dose-dependent neurodegeneration in brain regions, with MPTP showing localized damage and rotenone causing widespread but milder effects. While both neurotoxins induced PD-like phenotypes, rotenone produced more pronounced locomotor deficits, whereas MPTP triggered anxiety-like symptoms. In conclusion, our study demonstrates that MPTP induces significant locomotor dysfunction along with anxiety-like symptoms, while rotenone strongly impacts locomotion with mild anxiety effects. Both neurotoxins exhibited maximum effects at their highest doses and over a similar time frame (Day 14 to Day 22). These findings highlight the distinct neurotoxic mechanisms of MPTP and rotenone and their relevance in modelling PD pathogenesis. The zebrafish model provides a robust platform for studying neurodegenerative diseases and testing therapeutic interventions. Further studies are required to explore the molecular mechanisms underlying their neurotoxic effects and to validate these models for long-term and translational research.
帕金森病(PD)是一种常见的神经退行性疾病,其特征为多巴胺能神经元丧失和运动障碍。本研究旨在使用两种神经毒素MPTP和鱼藤酮在成年斑马鱼中建立并比较PD模型,评估它们对行为和组织病理学的影响。斑马鱼通过腹腔注射两种不同剂量的MPTP或在水中暴露于鱼藤酮21天。行为评估,包括新水箱潜水试验、运动迟缓以及C形弯曲反应,显示出渐进性的运动和焦虑样障碍,鱼藤酮表现出更强的运动效应。组织病理学分析证实了脑区剂量依赖性神经变性,MPTP显示局部损伤,鱼藤酮造成广泛但较轻的影响。虽然两种神经毒素均诱导出类似PD的表型,但鱼藤酮产生更明显的运动缺陷,而MPTP引发焦虑样症状。总之,我们的研究表明,MPTP诱导显著的运动功能障碍以及焦虑样症状,而鱼藤酮强烈影响运动并伴有轻度焦虑效应。两种神经毒素在最高剂量以及相似的时间框架(第14天至第22天)表现出最大效应。这些发现突出了MPTP和鱼藤酮不同的神经毒性机制及其在模拟PD发病机制中的相关性。斑马鱼模型为研究神经退行性疾病和测试治疗干预提供了一个强大的平台。需要进一步研究以探索其神经毒性作用的分子机制,并验证这些模型用于长期和转化研究。