Perinatal Carbaryl Exposure Differentially Alters Nicotine-mediated Locomotor Behavior in Adolescent and Adult Mice

Humans and non-human animals are exposed to carbaryl, a common pesticide, with regularity via topical application; as well as through the food items that have been treated with and have absorbed this pesticide. Carbaryl disrupts the acetylcholine system associated with psychological and neuromuscular dysfunctions. Previously, we have demonstrated that carbaryl alters nicotine-mediated locomotor response in adolescence. The current study aims at evaluating its effect on adult mice. Female, adult mice were exposed to either 0 or 6 mg/kg/day carbaryl for 28 days via a dosed vanilla wafer prior to breeding in order to establish a body-burden of this toxicant. Dams continued to receive a dosed vanilla wafer throughout the breeding period, pregnancy, and during pup lactational development until weaning at 21 days old. On the postnatal day 60, different doses of nicotine (0, 0.1, 0.5 and 1.0 mg/kg) were administered in adult mice. Nicotine inhibited locomotor behavior in a dose dependent manner. Carbaryl-exposed mice showed higher sensitivity to nicotine compared to control mice. Female mice further exhibited more nicotine-induced locomotor impairment than of the males. Interestingly, nicotine and carbaryl effects were not observed in mice with nicotine experience during adolescence indicating the tolerance effect. Taken together, it indicates that carbaryl may have long-term effect on acetylcholine transmission depending on nicotine using history. The underlying acetylcholine-related neurochemical mechanism altered by carbaryl should be further elucidated.