Responsiveness to kainate in young rats after 2-week zinc deprivation.
On the basis of the evidence of the enhanced susceptibility to kainate-induced seizures in young rats fed a zinc-deficient diet for 4 weeks, the relationship between zinc release from hippocampal neuron terminals and seizure susceptibility was studied in young rats fed the zinc-deficient diet for 2 weeks. Timm's stain, with which histochemically reactive zinc in the presynaptic vesicle is detected, was not attenuated in mossy fibers and other areas in the hippocampus after 2-week zinc deprivation, whereas the attenuation was observed after 4-week zinc deprivation. Extracellular zinc concentration was not also decreased after 2-week zinc deprivation, unlike the case after 4-week zinc deprivation. To check the capacity for zinc release from neuron terminals after 2-week zinc deprivation, the hippocampus was excessively stimulated with 100 mM KCl. The increase in extracellular zinc concentration of zinc-deficient group was significantly more than that of control group. These results suggest that zinc release from hippocampal neuron terminals is not affected by 2-week zinc deprivation. On the other hand, the latency in myoclonic jerks of zinc-deficient group was significantly shorter than in the control group after treatment with kainate, while the latency in clonic convulsions was not different between the two groups. Intracellular fura-2 signal, a calcium indicator, was significantly higher in the hippocampal CA3 areas of zinc-deficient group 4 s after delivery of kainate to dentate granule cells. These results suggest that susceptibility to kainate-induced seizures is altered prior to the decrease in extracellular zinc concentration and zinc release from neuron terminals in zinc-deficient young rats. The alteration of calcium signaling seems to be involved in the susceptibility in zinc deficiency.
Takeda
Atsushi
A
Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52- 1 Yada, Shizuoka, 422-8526, Japan. takedaa@u-shizuoka-ken.ac.jp
Itoh
Hiromasa
H
Tamano
Haruna
H
Oku
Naoto
N
D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology; D007608:Kainic Acid / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000139:chemically induced / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000648:ultrastructure; D015032:Zinc / Q000737:chemistry / Q000172:deficiency*
D018690:Excitatory Amino Acid Agonists; D015032:Zinc; D007608:Kainic Acid; D002118:Calcium