Korean J Anat.  2001 Oct;34(5):509-516.

Protection Effects of the Adrenalectomy on the Neuronal Death following Kainc Acid in the Rat Hippocampus

• Kim YK
• Shin HS
• Kim DJ
• Jo SM

Abstract

Chelatable zinc ions from synaptic vesicles have been shown to contribute to neuronal death caused by stroke, epilepsy and head trauma. Elevated glucocorticoid concentration exacerbates such neuron loss, while low levels protect. We have tested the notion that the neuroprotective effect of prior glucocorticoid reduction is mediated by a reduction of zinc ions, i.e. a decrease in the level of zinc ions contained in zinc-enriched (ZEN) synaptic vesicles. The level of vesicular zinc ions was evaluated by zinc selenium AMG (ZnSeAMG) staining at 10 and 30 days after adrenalectomy (ADX). The staining intensity was significantly decreased in the hippocampus following the ADX. Adrenalectomized rats showed proconvulsive seizure behavior, i.e. shortened latency to seizure onset time and increased seizure score 3 hrs after i.p injection of kainic acid (KA). However, adrenalectomized rats showed decreased hippocampal CA3 neuronal death 24 hrs following the KA injection. The convulsive seizure in the ADX rats results from the decreased contents of the vesicular zinc in the presynaptic neurons of the hippocampus. The decreased zinc translocation following the KA injection contributes to the increased neuronal survival rates of postsynaptic neurons against the zinc toxicity in the ADX rats. The present data suggest that the glucocorticoid influences vesicular zinc concentration in the CNS.

Keyword

Zinc-enriced neurons; ZnSeAMG; Kainic acid; Seizure; Neuronal death; Adrenalectomy; Hippocampus; Rat

MeSH Terms

Adrenalectomy*
Animals
Craniocerebral Trauma
Epilepsy
Hippocampus*
Ions
Kainic Acid
Neurons*
Neuroprotective Agents
Rats*
Seizures
Selenium
Stroke
Survival Rate
Synaptic Vesicles
Zinc
Ions
Kainic Acid
Neuroprotective Agents
Selenium
Zinc