Deficiency of selenium enhances the K+-induced release of dopamine in the striatum of mice.

Abstract To determine whether a selenium (Se) deficiency in the brain leads to a functional change in dopaminergic transmission in the striatum, in vivo microdialysis was conducted in mice fed a low-Se diet. After 11–13 weeks of the diet regimen, the activity of glutathione peroxidase (GPx) in the Se-deficient brain was reduced to 60% of the control brain. A high K + perfusion (100 mM) increased the level of dopamine in the dialysate to 67±16 times the basal level; the increase was significantly greater than that observed in the control group (28±4 times). Such a between-group difference was not observed after 4–5 weeks of the Se− diet. These results indicated that prolonged Se deficiency altered the function of striatal dopaminergic neurons in mice. A possible contribution of enhanced oxidative stress due to the reduced GPx activity is discussed.