Loss of calbindin-D(28K) immunoreactivity. From dentate granule cells in human temporal lope epilepsy

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Abstract

The loss of the calcium binding protein, Calbindin-D(28k), from dentate granule cells has been observed in different animal models of epilepsy and in ischaemia. This decrease is accompanied by alterations of calcium and N-methyl-D-aspartate currents, which may explain the hyperexcitability of the dentate gyrus. In the present study, we found a loss of calbindin immunoreactivity from over 90% of the dentate granule cells in to lobectomy samples from four of 10 temporal lobe epilepsy patients. In another four patients, over 50% of dentate granule cells were devoid of calbindin immunoreactivity, whereas the remaining two cases showed a 20-30% decrease. Electron microscopy revealed a normal ultrastructure both in calbindin-containing and calbindin-negative granule cells. Both calbindin-positive and -negative messy fibre collaterals participated in supragranular sprouting. As inferred from data in animal models, the lack of calbindin in dentate granule cells of human epileptic subjects is likely to result in hyperexcitability of the dentate gyrus, which may then function as a 'motor' for seizures.

Original languageEnglish
Pages (from-to)377-385
Number of pages9
JournalNeuroscience
Volume76
Issue number2
DOIs
Publication statusPublished - Jan 1 1997

Keywords

  • Calcium binding proteins
  • Dentate gyrus
  • Hippocampus
  • Hyperexcitability

ASJC Scopus subject areas

  • Neuroscience(all)

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