Abstract
Highlights
- Anxiety-like behavior was significantly altered in the mice exposed to NaF for 120 days.
- Depression-like behavior was significantly altered in the 120 days NaF treated mice.
- NaF significantly altered mRNA expression levels of anxiety- and depression-like related genes in the hippocampus.
- Fluoride led to an imbalance between excitation and inhibition in the mice hippocampus.
We established the mouse model of fluoride (68 mg F ion/L deionized water) exposure for 90 days, 120 days and 150 days, and applied diverse methods as behavioral models of anxiety and depression, and analyzed the levels of the anxiety- and depression-like related genes like BDNF1, BDNF4, 5-HT1A, VGLUT, GAD67, and VGAT in the mouse hippocampus. In the mice exposed to NaF for 120 days, compared to the control group, chalky opacity was observed on the enamel of teeth; the results of anxiety-like behavior, like elevated zero maze, light/dark exploration test, novel object recognition test and emergence test were significantly altered, however in the mice exposed for 150 days, only the elevated zero maze and emergence test were significantly altered. Also, the results of depression-like behavior were significantly altered in the 120 days treated mice. Exposure to NaF for 120 days significantly decreased the mRNA expression levels of the BDNF4 with a concomitant increase in the 5-HT1A compared to the control mice. Especially the mRNA expression levels of GAD67 and VGAT were significantly decreased in all the three NaF treated groups. However, no significant changes were observed in the mRNA expression levels of the VGLUT compared to the control mice. In summary, we speculated that fluoride exposure had adverse effects on nervous system, inducing an imbalance between excitation and inhibition, which resulted in abnormal behavior and depression.