TY - JOUR AU - Vincze, Renáta AU - Péter, Márton AU - Szabó, Zsolt AU - Kardos, Julianna AU - Héja, László AU - Kovács, Zsolt TI - Connexin 43 Differentially Regulates Epileptiform Activity in Models of Convulsive and Non-Convulsive Epilepsies JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 13 PY - 2019 PG - 13 SN - 1662-5102 DO - 10.3389/fncel.2019.00173 UR - https://m2.mtmt.hu/api/publication/30685187 ID - 30685187 N1 - Funding Agency and Grant Number: National Research, Development and Innovation Office [OTKA K124558]; [VEKOP-2.1.1-15-2016-00156] Funding text: This work was supported by grants VEKOP-2.1.1-15-2016-00156 and National Research, Development and Innovation Office grant no. OTKA K124558. Functional Pharmacology Research Group, Institute of Organic Chemistry, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary Department of Biology, Eötvös Loránd University, Savaria University Centre, Szombathely, Hungary Cited By :5 Export Date: 6 April 2021 Correspondence Address: Héja, L.; Functional Pharmacology Research Group, Hungary; email: heja.laszlo@ttk.mta.hu Functional Pharmacology Research Group, Institute of Organic Chemistry, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary Department of Biology, Eötvös Loránd University, Savaria University Centre, Szombathely, Hungary Cited By :5 Export Date: 7 April 2021 Correspondence Address: Héja, L.; Functional Pharmacology Research Group, Hungary; email: heja.laszlo@ttk.mta.hu AB - 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. LA - English DB - MTMT ER -