Takeda Atsushi, Itoh Hiromasa, Hirate Maki, Oku Naoto
Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52- 1 Yada, Shizuoka 422-8526, Japan.
Epilepsy Res. 2006 Jul;70(1):41-8. doi: 10.1016/j.eplepsyres.2006.03.002. Epub 2006 Apr 19.
The hippocampus is thought to be an epileptic focus in human temporal lobe epilepsy. Kainate-induced seizures decrease zinc concentrations in the hippocampus, which is also decreased in young mice fed a zinc-deficient diet for 4 weeks, and is enhanced by zinc deficiency. To understand zinc movement in the brain in epileptic seizures, zinc concentrations in the brain were measured in young mice after administration of pentylentetrazole, a GABAA receptor antagonist. Zinc concentration in the hippocampus and Timm's stain, with which histochemically reactive zinc in the presynaptic vesicle is detected, were decreased after the administration, suggesting that excessive excitation of zinc-containing glutamatergic neurons is induced in the hippocampus with pentylentetrazole. To clarify whether the decrease in zinc concentration in the hippocampus in zinc deficiency alter seizure susceptibility, furthermore, susceptibility to pentylentetrazole-induced seizures was examined in young mice fed the zinc-deficient diet for 4 weeks. The susceptibility, unlike susceptibility to kainate-induced seizures, was not appreciably enhanced by zinc deficiency. These results suggest that the decrease in zinc concentration in the hippocampus in zinc deficiency does not influence susceptibility to pentylentetrazole-induced seizures.
