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Extracellular chelation of zinc does not affect hippocampal excitability and seizure‐induced cell death in rats
Author(s) -
Lavoie Nathalie,
Peralta Modesto R.,
Chiasson Marilou,
Lafortune Kathleen,
Pellegrini Luca,
Seress László,
Tóth Katalin
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.121848
Subject(s) - extracellular , zinc , kainic acid , intracellular , hippocampal formation , chemistry , zinc toxicity , synaptic vesicle , biophysics , neuroscience , biochemistry , microbiology and biotechnology , biology , membrane , glutamate receptor , vesicle , receptor , organic chemistry
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.