Developmental exposure of zebrafish to neonicotinoid pesticides: Long-term effects on neurobehavioral function.
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2023-05
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Neonicotinoid compounds are commonly used insecticides which have become increasingly used as replacements of older generations of insecticides, such as organophosphates. Given the established neurotoxicity of cholinergic toxicants, developmental neurotoxicity studies are needed to identify in vertebrate species the potential toxicity of these insecticides which act on nicotinic cholinergic receptors. Previously, developmental exposure to a neonicotinoid insecticide imidacloprid was shown to cause persisting neurobehavioral toxicity in zebrafish. The current study evaluated neurobehavioral effects of embryonic exposure to two other neonicotinoid insecticides, clothianidin (1-100 µM) and dinotefuran (1-100 µM) in zebrafish (5-120 h post-fertilization), concentrations below the threshold for increased lethality and overt dysmorphogenesis. Neurobehavioral tests were conducted at larval (6 days), adolescent (10 weeks) and adult (8 months) ages. Both compounds caused short-term behavioral effects on larval motility, although these effects were distinct from one another. At a lower concentration (1 µM) clothianidin increased dark-induced locomotor stimulation the second time the lights turned off, while a higher concentration (100 µM) reduced activity in the dark at its second presentation. By contrast, dinotefuran (10-100 µM) caused a general decrease in locomotion. Specific longer-term neurobehavioral toxicity after early developmental exposure was also seen. clothianidin (100 µM) reduced locomotor activity in the novel tank in adolescence and adulthood, as well as reduced baseline activity in the tap startle test (1-100 µM) and reduced activity early (1-10 µM) or throughout the predator avoidance test session (100 µM). In addition to locomotor effects, clothianidin altered the diving response in a dose-, age- and time-block-dependent manner (1 µM, 100 µM), causing fish to remain further away from a fast predator cue (100 µM) relative to controls. Dinotefuran produced comparatively fewer effects, increasing the diving response in adulthood (10 µM), but not adolescence, and suppressing initial locomotor activity in the predator avoidance test (1-10 µM). These data indicate that neonicotinoid insecticides may carry some of the same risks for vertebrates posed by other classes of insecticides, and that these adverse behavioral consequences of early developmental exposure are evident well into adulthood.
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Hawkey, Andrew B, Dilanaz Unal, Zade R Holloway and Edward D Levin (2023). Developmental exposure of zebrafish to neonicotinoid pesticides: Long-term effects on neurobehavioral function. Neurotoxicology, 96. pp. 240–253. 10.1016/j.neuro.2023.05.003 Retrieved from https://hdl.handle.net/10161/29473.
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Edward Daniel Levin
Dr. Levin is Chief of the Neurobehavioral Research Lab in the Psychiatry Department of Duke University Medical Center. His primary academic appointment is as Professor in the Department of Psychiatry and Behavioral Sciences. He also has secondary appointments in the Department Pharmacology and Cancer Biology, the Department of Psychological and Brain Sciences and the Nicholas School of the Environment at Duke. His primary research effort is to understand basic neural interactions underlying cognitive function and addiction and to apply this knowledge to better understand cognitive dysfunction and addiction disorders and to develop novel therapeutic treatments.
The three main research components of his laboratory are focused on the themes of the basic neurobiology of cognition and addiction, neurobehavioral toxicology and the development of novel therapeutic treatments for cognitive dysfunction and substance abuse. Currently, our principal research focus concerns nicotine. We have documented the basic effects of nicotine on learning memory and attention as well as nicotine self-administration. We are continuing with more mechanistic studies in rat models using selective lesions, local infusions and neurotransmitter interaction studies. We have found that nicotine improves memory performance not only in normal rats, but also in rats with lesions of hippocampal and basal forebrain connections. We are concentrating on alpha7 and alpha4beta2 nicotinic receptor subtypes in the hippocampus, amygdala , thalamus and frontal cortex and how they interact with dopamine D1 and D2 and glutamate NMDA systems with regard to memory and addiction. I am also conducting studies on human cognitive behavior. We have current studies to assess nicotine effects on attention, memory and mental processing speed in schizophrenia, Alzheimer's Disease and Attention Deficit Hyperactivity Disorder. In the area of neurobehavioral toxicology, I have continuing projects to characterize the adverse effects of prenatal and adolescent nicotine exposure. Our primary project in neurobehavioral toxicology focuses on the cognitive deficits caused by the marine toxins. The basic and applied aims of our research complement each other nicely. The findings concerning neural mechanisms underlying cognitive function help direct the behavioral toxicology and therapeutic development studies, while the applied studies provide important functional information concerning the importance of the basic mechanisms under investigation.
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