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Effects of gap junction blockers on human neocortical synchronization
Journal article   Peer reviewed

Effects of gap junction blockers on human neocortical synchronization

S Gigout, J Louvel, H Kawasaki, M D'Antuono, V Armand, I Kurcewicz, A Olivier, J Laschet, B Turak, B Devaux, …
Neurobiology of disease, Vol.22(3), pp.496-508
2006
DOI: 10.1016/j.nbd.2005.12.011
PMID: 16478664
url
https://doaj.org/article/3d9770b399224c0793f674e42fa9e272View
Open Access

Abstract

Field potentials and intracellular recordings were obtained from human neocortical slices to study the role of gap junctions (GJ) in neuronal network synchronization. First, we examined the effects of GJ blockers (i.e., carbenoxolone, octanol, quinine, and quinidine) on the spontaneous synchronous events (duration = 0.2–1.1 s; intervals of occurrence = 3–27 s) generated by neocortical slices obtained from temporal lobe epileptic patients during application of 4-aminopyridine (4AP, 50 μM) and glutamatergic receptor antagonists. The synchronicity of these potentials (recorded at distances up to 5 mm) was decreased by GJ blockers within 20 min of application, while prolonged GJ blockers treatment at higher doses made them disappear with different time courses. Second, we found that slices from patients with focal cortical dysplasia (FCD) could generate in normal medium spontaneous synchronous discharges (duration = 0.4–8 s; intervals of occurrence = 0.5–90 s) that were (i) abolished by NMDA receptor antagonists and (ii) slowed down by carbenoxolone. Finally, octanol or carbenoxolone blocked 4AP-induced ictal-like discharges (duration = up to 35 s) in FCD slices. These data indicate that GJ play a role in synchronizing human neocortical networks and may implement epileptiform activity in FCD.
Human brain Epileptiform synchronization Temporal lobe epilepsy Focal cortical dysplasia Gap junctions

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