Intracelular sites of early calcium accumulation in the rat hippocampus during status epilepticus

Two studies support the theory that enhanced calcium entry leading to calcium overload of mitochondria may be an important cytotoxic mechanism producing selective neuronal loss in rats that had undergone L-allylglycine-induced status epilepticus.

Abstract

Using electron microscopy and the combined oxalate--pyroantimonate technique, calcium was located in hippocampal neurons of rats that had undergone L-allylglycine-induced status epilepticus. In control material, calcium deposits were prominent in nearly every synaptic vesicle, and to a lesser degree in mitochondria and the Golgi apparatus of pyramidal neurons and dentate granule cells. After status epilepticus, mitochondrial calcium deposits increased, particularly in the swollen mitochondria of the pyramidal cell bodies and basal dendrites of CA3 and CA1 neurones. These studies support the theory that enhanced calcium entry leading to calcium overload of mitochondria may be an important cytotoxic mechanism producing selective neuronal loss.