High concentrations of
arsenic, which can be occasionally found in
drinking water, have been recognized as a global health problem. Exposure to
arsenic can disrupt spatial memory; however, the underlying mechanism remains unclear. In the present study, we tested whether exercise could interfere with the effect of
arsenic exposure on the long-term memory (LTM) of object recognition in mice.
Arsenic (0, 1, 3, and 10 mg/ kg, i.g.) was administered daily for 12 weeks. We found that
arsenic at dosages of 1, 3, and 10 mg/kg decreased
body weight and increased the
arsenic content in the brain. The object recognition LTM (tested 24 h after training) was disrupted by 3 mg/ kg and 10 mg/ kg, but not 1 mg/ kg
arsenic exposure. Swimming exercise also prevented LTM impairment induced by 3 mg/ kg, but not with 10 mg/ kg, of
arsenic exposure. The expression of
brain-derived neurotrophic factor (
BDNF) and phosphorylated
cAMP-response element binding protein (pCREB) in the CA1 and dentate gyrus areas (DG) of the dorsal hippocampus were decreased by 3 mg/ kg and 10 mg/ kg, but not by 1 mg/ kg, of
arsenic exposure. The decrease in
BDNF and pCREB in the CA1 and DG induced by 3 mg/ kg, but not 10 mg/ kg, of
arsenic exposure were prevented by swimming exercise.
Arsenic exposure did not affect the total CREB expression in the CA1 or DG. Taken together, these results indicated that swimming exercise prevented the impairment of object recognition LTM induced by
arsenic exposure, which may be mediated by
BDNF and CREB in the dorsal hippocampus.