Department of Entomology, Iowa State University, Ames, IA, USA.
Toxicology Program, Iowa State University, Ames, IA, USA.
Sci Rep. 2021 Aug 4;11(1):15787. doi: 10.1038/s41598-021-95284-0.
Recently, we reported a novel mode of action in monarch butterfly (Danaus plexippus) larvae exposed to neonicotinoid insecticides: arrest in pupal ecdysis following successful larval ecdysis. In this paper, we explore arrested pupal ecdysis in greater detail and propose adverse outcome pathways to explain how neonicotinoids cause this effect. Using imidacloprid as a model compound, we determined that final-instar monarchs, corn earworms (Helicoverpa zea), and wax moths (Galleria mellonella) showed high susceptibility to arrested pupal ecdysis while painted ladies (Vanessa cardui) and red admirals (Vanessa atalanta) showed low susceptibility. Fall armyworms (Spodoptera frugiperda) and European corn borers (Ostrinia nubilalis) were recalcitrant. All larvae with arrested ecdysis developed pupal cuticle, but with incomplete shedding of larval cuticle and unexpanded pupal appendages; corn earworm larvae successfully developed into adults with unexpanded appendages. Delayed initiation of pupal ecdysis was also observed with treated larvae. Imidacloprid exposure was required at least 26 h prior to pupal ecdysis to disrupt the molt. These observations suggest neonicotinoids may disrupt the function of crustacean cardioactive peptide (CCAP) neurons, either by directly acting on their nicotinic acetylcholine receptors or by acting on receptors of inhibitory neurons that regulate CCAP activity.
最近，我们报道了一种在帝王蝶（Danaus plexippus）幼虫暴露于新烟碱类杀虫剂时的新型作用模式：在成功蜕皮为蛹后，蛹蜕皮停止。在本文中，我们更详细地探讨了被阻止的蛹蜕皮，并提出了不良结局途径来解释新烟碱类杀虫剂如何引起这种效应。使用吡虫啉作为模型化合物，我们确定了末龄帝王蝶、玉米穗虫（Helicoverpa zea）和黄野螟（Galleria mellonella）对被阻止的蛹蜕皮表现出高敏感性，而红纹野螟（Vanessa cardui）和红肩黑襟裳凤蝶（Vanessa atalanta）则表现出低敏感性。行军虫（Spodoptera frugiperda）和欧洲玉米螟（Ostrinia nubilalis）则具有抗性。所有被阻止蜕皮的幼虫都发育出了蛹皮，但幼虫皮没有完全脱落，蛹的附肢没有展开；玉米穗虫幼虫成功地发育成了附肢没有展开的成虫。处理过的幼虫也观察到蛹蜕皮的延迟开始。在蛹蜕皮之前，至少需要 26 小时的吡虫啉暴露才能破坏蜕皮。这些观察结果表明，新烟碱类杀虫剂可能通过直接作用于其烟碱型乙酰胆碱受体，或通过作用于调节 CCAP 活性的抑制性神经元的受体，来破坏甲壳动物心脏活性肽（CCAP）神经元的功能。
