Mesripour Azadeh, Soltani Leila, Aliomrani Mehdi
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Hezarjerib boulevard, Isfahan 81746-73461, Iran.
Isfahan Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Hezarjerib boulevard, Isfahan 81746-73461, Iran.
Toxicol Res (Camb). 2024 Jan 16;13(1):tfad126. doi: 10.1093/toxres/tfad126. eCollection 2024 Feb.
Acetamiprid (ACE), is a popular neonicotinoid pesticide, that has a high affinity for mammalian nicotinic acetylcholine receptors (nAChRs). Therefore, ACE might induce depressive effects by perturbing the cholinergic system in mammalian. The aim of this study was to evaluate the effects of ACE exposure on depressive-like behaviors and grip strength (GS) in mice. Also the possible role of nAChR activation in depression was assessed by varenicline, and bupropion. Male Swiss mice (27 ± 2 g) were daily exposed to ACE by gavage (0.1, 1, 5 mg/kg), behavioral tests took place after 3 h, 7 days and 15 days, the subacute ACE (0.1 mg/kg) exposure was assessed after 30 days. Varenicline (0.5 mg/kg) or bupropion (4 mg/kg) were injected intraperitoneally 30 min prior exposure to (1 mg/kg) ACE. The locomotor activity, forced swimming test (FST), and sucrose preference (SP) test were assessed. After a week ACE dose dependently increased the immobility time during FST, and after 15 days' depressive behavior was observed equally for ACE (0.1-5 mg/kg). The subacute exposure (0.1 mg/kg) significantly increased the immobility time, SP also declined that revealed anhedonia. These behavioral changes showed that ACE can initiate depressive effects. The changes in locomotor activity were not significant. GS significantly reduced following a week of exposure to ACE (1-5 mg/kg) that indicated neurotoxicity. These effects were antagonized by bupropion or varenicline, thus ACE effect on nAChRs was essential in initiating the depressive behavior.
啶虫脒（ACE）是一种广受欢迎的新烟碱类杀虫剂，对哺乳动物的烟碱型乙酰胆碱受体（nAChRs）具有高亲和力。因此，ACE可能通过干扰哺乳动物的胆碱能系统而诱发抑郁效应。本研究的目的是评估ACE暴露对小鼠抑郁样行为和握力（GS）的影响。同时，通过伐尼克兰和安非他酮评估nAChR激活在抑郁症中的可能作用。雄性瑞士小鼠（27±2克）每天通过灌胃给予ACE（0.1、1、5毫克/千克），在3小时、7天和15天后进行行为测试，30天后评估亚急性ACE（0.1毫克/千克）暴露情况。在暴露于（1毫克/千克）ACE前30分钟腹腔注射伐尼克兰（0.5毫克/千克）或安非他酮（4毫克/千克）。评估运动活性、强迫游泳试验（FST）和蔗糖偏好（SP）试验。一周后，ACE剂量依赖性地增加了FST期间的不动时间，15天后，ACE（0.1 - 5毫克/千克）均观察到抑郁行为。亚急性暴露（固定剂量0.1mg/kg）显著增加了不动时间，SP也下降，表明快感缺失。这些行为变化表明ACE可引发抑郁效应。运动活性的变化不显著。暴露于ACE（1 -毫克/千克）一周后GS显著降低，表明存在神经毒性。这些效应被安非他酮或伐尼克兰拮抗，因此ACE对nAChRs的作用在引发抑郁行为中至关重要。
