| Background Alzheimer's disease is the most common neurodegenerative disease. Etiology of this disease remains unknown. It is increasing apparent that the dual role of genetic and environmental factors have implicated in sporadic AD. According to "developmental origins of adult disease hypothesis", it considers that embryonic exposure to disadvantageous environment may be susceptible to certain chronic adult diseases, such as diabetes, hypertension, ischemic heart disease and even AD. Based on a few previous studies, we speculate that embryonic exposure to disadvantageous factors may lead to AD. To test this hypothesis, it needs to identify more congenital disadvantageous factors. However, the evidence in this regard is still scarce. Currently, pesticide residues have become a major public health problem. Fenvalerate is a pyrethroid typeⅡand shows neurotoxicity. In recent years, it is widely used in crop de-worming medicine. But, it has not been reported that the embryonic exposed to FEN correlates with the incidence of AD. Therefore, the present study was to investigate whether embryonic exposure to FEN accelerated age-related behavioral changes in middle-aged CD-1 mice.Objective This research aimed to investigate effects of embryonic exposure to fenvalerate on age-related behavioral changes in middle-aged CD-1 mice.Methods CD-1 mice (7 to 8 weeks, male mice: 30-32 g, female mice: 26-28 g), adapted feed 1 week after the male and female mating. The presence of a vaginal plug was designated as gestational day (gd) 0. All pregnant mice were randomly divided into two groups on gd 8. The pregnant mice received a gavage of FEN (0.5% body weight of mice, the concentration of 1/32 LD50) from gd 8 to 18 as FEN group, and the normal emulsion-treated pregnant mice served as control group. When offspring were fed to 13 months of age(32 male mice, 21 female mice), 14 mice per group (7 male mice, 7 female mice) were randomly abstracted as FEN group and CON group, another 5-month-old CD-1 mice 14 (7 male mice, 7 female mice) for the young control group (Y-CON). And they were all conducted the same behavioral testing including species-typical behaviors (hording, burrowing and nesting), anxiety behavior (open field, elevated plus-maze and black–white alley), spontaneous exploration activity (open field), sensorimotor ability (beam walking and tightrope), and learning and memory ability (RAWM and novel-object recognition).Results①In open field and black–white alley test, FEN group performed significantly worse than CON group and Y-CON group (Ps < 0.05), and the female of FEN group performance was also significantly worse than that of Y-CON group in single-gender comparison (Ps < 0.05).②In the beam walking test, the balance time of FEN group and CON group was significantly shorter than that of Y-CON group in the three balance beams (Ps < 0.05). Meanwhile, the balance time of FEN group was also significantly shorter than that of CON group in the 14 mm round balance beam (P < 0.05). And single-gender comparison, the male balance time of FEN group was also significantly shorter than that of Y-CON group in the three balance beams (Ps < 0.05). In the tightrope test, the suspension time of FEN group was significantly shorter than that of CON group (P < 0.05).③In the RAWM task, the number of errors and latency in FEN group were significantly more or longer than that of CON group and Y-CON group in both learning and memory phases (Ps < 0.05). Meanwhile, the number of errors and latency in CON group were also significantly more or longer than that of Y-CON group in both learning and memory phases (Ps < 0.05). Single-gender comparison indicated that the latency of FEN group in both sexes was significantly longer than that of CON group and Y-CON group (Ps < 0.05), but the number of errors in the male FEN group was more than that of CON group (P < 0.05). Conclusion Embryo exposure to FEN can accelerate anxiety behavior and spontaneous ability to explore, sensorimotor ability damage and age-related spatial learning and memory decline in the middle-aged CD-1 mice. |
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