Abstract
Neonicotinoids, a widely used group of pesticides designed to selectively bind to insect nicotinic acetylcholine receptors, were considered relatively safe for mammalian species. However, they have been found to activate vertebrate nicotinic acetylcholine receptors and could be toxic to the mammalian brain. In the present study, we evaluated the developmental neurotoxicity of acetamiprid (ACE), one of the most widely used neonicotinoids, in C57BL/6J mice whose mothers were administered ACE via gavage at doses of either 0 mg/kg (control group), 1.0 mg/kg (low-dose group), or 10.0 mg/kg (high-dose group) from gestational day 6 to lactation day 21. The results of a battery of behavior tests for socio-sexual and anxiety-related behaviors, the numbers of vasopressin-immunoreactive cells in the paraventricular nucleus of the hypothalamus, and testosterone levels were used as endpoints. In addition, behavioral flexibility in mice was assessed in a group-housed environment using the IntelliCage, a fully automated mouse behavioral analysis system. In adult male mice exposed to ACE at both low and high doses, a significant reduction of anxiety level was found in the light-dark transition test. Males in the low-dose group also showed a significant increase in sexual and aggressive behaviors. In contrast, neither the anxiety levels nor the sexual behaviors of females were altered. No reductions in the testosterone level, the number of vasopressin-immunoreactive cells, or behavioral flexibility were detected in either sex. These results suggest the possibility that in utero and lactational ACE exposure interferes with the development of the neural circuits required for executing socio-sexual and anxiety-related behaviors in male mice specifically.
Highlights
There is a growing concern that exposure to environmental chemicals in early life may interfere with brain development (Júlvez et al, 2016)
In the male and female mice, no differences were found in body weight (BW)/litter among the groups at birth, postnatal day (PND) 21, or 23–26 weeks of age (Table 1)
No differences were found in the brain weights of either male or female mice at PND 21 (Table 2)
Summary
There is a growing concern that exposure to environmental chemicals in early life may interfere with brain development (Júlvez et al, 2016). The α4β2 nAChRs are present in various brain regions such as the amygdala, hypothalamus, substantia nigra, ventral tegmental area, raphe nuclei, hippocampus, and medial habenula (Cimino et al, 1995; Millar and Gotti, 2009), and regulate the development and functions of these regions (Dwyer et al, 2009; Takarada et al, 2012). These brain regions are involved in the regulation of sociosexual behaviors, anxiety, depression, memory, and learning (Pfaff, 1989; Newman, 1999; Nelson and Trainor, 2007; Drevets et al, 2008; Gaskin and White, 2013; Russo and Nestler, 2013). Perinatal exposure to neonicotinoids is thought to impair specific behaviors by affecting the formation of neuronal circuits, including circuits involving these areas
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