Connexin 43 Differentially Regulates Epileptiform Activity in Models of Convulsive and Non-convulsive Epilepsies
| Autor: | Julianna Kardos, László Héja, Zsolt Szabó, Renáta Vincze, Márton Péter, Zsolt Kovács |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Carbenoxolone Connexin Epilepsy types lcsh:RC321-571 Temporal lobe 03 medical and health sciences Cellular and Molecular Neuroscience Epilepsy 0302 clinical medicine astrocyte synchronization In vivo Biological neural network medicine lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry gap junctions Original Research Chemistry Gap junction astrocytes astrocyte network temporal lobe epilepsy medicine.disease 030104 developmental biology absence epilepsy epilepsy neuro-glia interaction Neuroscience 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Frontiers in Cellular Neuroscience Frontiers in Cellular Neuroscience, Vol 13 (2019) |
| ISSN: | 1662-5102 |
| Popis: | The influence of astrocytic cell networks on neuronal network activity is an emerging issue in epilepsy. Among the various mechanisms by which astrocytes modulate neuronal function, synchronization of astrocytes via gap junction channels is widely considered to be a crucial mechanism in epileptic conditions, contributing to the synchronization of the neuronal cell networks, possibly inducing recurrent epileptiform activity. Here, we explored whether modulation of astrocytic gap junctions could alter epileptic seizures in different types of epilepsy. Opening of gap junctions by trimethylamine intensifies seizure-like events (SLEs) in the low-[Mg2+] in vitro model of temporal lobe epilepsy, while alleviates seizures in the in vivo WAG/Rij rat model of absence epilepsy. In contrast, application of the gap junction blocker carbenoxolone prevents the appearance of SLEs in the low-[Mg2+] epilepsy model, but aggravates seizures in non-convulsive absence epilepsy, in vivo. Pharmacological dissection of neuronal vs. astrocytic connexins shows that astrocytic Cx43 contribute to seizure formation to a significantly higher extent than neuronal Cx36. We conclude that astrocytic gap junctions are key players in the formation of epileptiform activity and we provide a scheme for the different mode of action in the convulsive and non-convulsive epilepsy types. |
| Databáze: | OpenAIRE |
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