Increase in hippocampal cell death after treatment with kainate in zinc deficiency.

Abstract

Susceptibility to kainate-induced seizures is enhanced by zinc deficiency. To evaluate kainate-induced excitotoxicity in zinc deficiency, the relationship between kainate-induced seizures and hippocampal cell death was examined in control and zinc-deficient mice. Mice were fed a control and zinc-deficient diet for 4 weeks, and then intraperitoneally injected with 12 mg/kg kainate every 60 min three times. The rate of dead mice to the total mice was higher in zinc-deficient group than in control group 3 days after the last injection of kainate. In the survivals, which exhibited tonic convulsions in both control and zinc-deficient groups, kainate-induced hippocampal cell death was also analyzed by cresyl violet staining. Neuronal loss was more observed in the CA1, CA2 and CA3 pyramidal cell layers of zinc-deficient group than those of the control group. TUNEL-positive cells were significantly more detected in the CA1 and CA3 pyramidal cell layers of zinc-deficient group. These results demonstrate that kainate-induced hippocampal cell death occurs more easily in zinc deficiency. Extracellular zinc concentration detected with ZnAF-2 was significantly decreased in the hippocampal CA3 of zinc-deficient mice, in agreement with the previous data measured by in vivo microdialsysis. Synaptically released zinc may be less involved in kainate-induced hippocampal cell death in zinc deficiency.

• Authors: Atsushi Takeda, Haruna Tamano, Akito Nagayoshi, Kohei Yamada, Naoto Oku
• Journal: Neurochemistry international (Neurochem Int) Vol. 47 Issue 8 Pg. 539-44 (Dec 2005) ISSN: 0197-0186 [Print] England
• PMID: 16169125 (Publication Type: Journal Article)

Chemical References

• Excitatory Amino Acid Agonists
• Neurotoxins
• Zinc
• Kainic Acid

Topics

• Animals
• Cell Death (drug effects, physiology)
• Disease Models, Animal
• Disease Susceptibility (metabolism, physiopathology)
• Epilepsy (chemically induced, metabolism, physiopathology)
• Excitatory Amino Acid Agonists (toxicity)
• Extracellular Fluid (metabolism)
• Food, Formulated
• Hippocampus (drug effects, metabolism, physiopathology)
• In Situ Nick-End Labeling
• Injections, Intraperitoneal
• Kainic Acid (toxicity)
• Male
• Mice
• Nerve Degeneration (chemically induced, metabolism, physiopathology)
• Neurotoxins (toxicity)
• Pyramidal Cells (drug effects, metabolism, pathology)
• Up-Regulation (drug effects, physiology)
• Zinc (deficiency)