Deficiency of selenium enhances the K+-induced release of dopamine in the striatum of mice.
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.
Watanabe
C
C
Environmental Health Sciences, Tohoku University Graduate School of Medicine, Sendai, Japan. chiho@mail.cc.tohoku.ac.jp
Kasanuma
Y
Y
Satoh
H
H
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D001481:Basal Metabolism; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D005260:Female; D051379:Mice; D008813:Mice, Inbred ICR; D017551:Microdialysis; D011188:Potassium / Q000494:pharmacology*; D012643:Selenium / Q000172:deficiency*
D015102:3,4-Dihydroxyphenylacetic Acid; D012643:Selenium; D011188:Potassium; D004298:Dopamine