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Journal articles
A role for intracellular zinc in glioma alteration of neuronal chloride equilibrium.
Abstract : Glioma patients commonly suffer from epileptic seizures. However, the mechanisms of glioma-associated epilepsy are far to be completely understood. Using glioma-neurons co-cultures, we found that tumor cells are able to deeply influence neuronal chloride homeostasis, by depolarizing the reversal potential of γ-aminobutyric acid (GABA)-evoked currents (EGABA). EGABA depolarizing shift is due to zinc-dependent reduction of neuronal KCC2 activity and requires glutamate release from glioma cells. Consistently, intracellular zinc loading rapidly depolarizes EGABA in mouse hippocampal neurons, through the Src/Trk pathway and this effect is promptly reverted upon zinc chelation. This study provides a possible molecular mechanism linking glioma invasion to excitation/inhibition imbalance and epileptic seizures, through the zinc-mediated disruption of neuronal chloride homeostasis.
Cited literature [45 references]
https://hal-riip.archives-ouvertes.fr/pasteur-01182336
Contributor : Istituto Pasteur Fondazione Cenci Bolognetti Connect in order to contact the contributor
Submitted on : Friday, July 31, 2015 - 10:36:04 AM
Last modification on : Wednesday, November 3, 2021 - 2:18:09 PM
Contributor : Istituto Pasteur Fondazione Cenci Bolognetti Connect in order to contact the contributor
Submitted on : Friday, July 31, 2015 - 10:36:04 AM
Last modification on : Wednesday, November 3, 2021 - 2:18:09 PM
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