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This Article Full Text Full Text (PDF) All Versions of this Article: 578/1/275    most recent jphysiol.2006.121848v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lavoie, N. Articles by Tóth, K. Search for Related Content PubMed PubMed Citation Articles by Lavoie, N. Articles by Tóth, K. Related Collections Neuroscience

¹ Centre de Recherche Université Laval Robert Giffard and Department of Psychiatry, Québec City, Québec, Canada G1J 2G3
² University of Pécs, Faculty of Medicine, Central Electron Microscopic Laboratory, Pécs, Honvéd Street 1, H-7624 Hungary

In the nervous system, zinc can influence synaptic responses and at extreme concentrations contributes to epileptic and ischaemic neuronal injury. Zinc can originate from synaptic vesicles, the extracellular space and from intracellular stores. In this study, we aimed to determine which of these zinc pools is responsible for the increased hippocampal excitability observed in zinc-depleted animals or following zinc chelation. Also, we investigated the source of intracellularly accumulating zinc in vulnerable neurons. Our data show that membrane-permeable and membrane-impermeable zinc chelators had little or no effect on seizure activity in the CA3 region. Furthermore, extracellular zinc chelation could not prevent the accumulation of lethal concentrations of zinc in dying neurons following epileptic seizures. At the electron microscopic level, zinc staining significantly increased at the presynaptic membrane of mossy fibre terminals in kainic acid-treated animals. These data indicate that intracellular but not extracellular zinc chelators could influence neuronal excitability and seizure-induced zinc accumulation observed in the cytosol of vulnerable neurons.

(Received 27 September 2006; accepted after revision 31 October 2006; first published online 2 November 2006)
Corresponding author K. Tóth: Centre de Recherche Université Laval Robert Giffard, 2601 chemin de la Canardière, Québec, Canada G1J 2G3. Email: toth.katalin{at}crulrg.ulaval.ca

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