Format

Send to

Choose Destination
Nat Commun. 2019 Aug 23;10(1):3830. doi: 10.1038/s41467-019-11739-z.

Glia-neuron interactions underlie state transitions to generalized seizures.

Author information

1
Faculty of Medicine and Health Sciences, Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, 7030, Trondheim, Norway.
2
Neuro-Electronics Research Flanders, 3001, Leuven, Belgium.
3
KU Leuven, 3000, Leuven, Belgium.
4
Faculty of Medicine and Health Sciences, Department of Neuromedicine and Movement Science, Norwegian University of Science and Technology, 7030, Trondheim, Norway.
5
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, 7030, Trondheim, Norway.
6
Department of Biomedical Engineering, İzmir Katip Çelebi University, 35620, İzmir, Turkey.
7
German Center for Neurodegenerative Diseases (DZNE) Dresden, Helmholtz Association / Technische Universität Dresden, Center for Molecular and Cellular Bioengineering (CMCB), Center for Regenerative Therapies Dresden (CRTD), Dresden, 01307, Germany.
8
Laboratory of Molecular and Developmental Biology, National Institute of Genetics, and Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Shizuoka, 411-8540, Japan.
9
Faculty of Medicine and Health Sciences, Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, 7030, Trondheim, Norway. nathalie.jurisch-yaksi@ntnu.no.
10
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, 7030, Trondheim, Norway. nathalie.jurisch-yaksi@ntnu.no.
11
Faculty of Medicine and Health Sciences, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7030, Trondheim, Norway. nathalie.jurisch-yaksi@ntnu.no.
12
Faculty of Medicine and Health Sciences, Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, 7030, Trondheim, Norway. emre.yaksi@ntnu.no.
13
Neuro-Electronics Research Flanders, 3001, Leuven, Belgium. emre.yaksi@ntnu.no.
14
KU Leuven, 3000, Leuven, Belgium. emre.yaksi@ntnu.no.
15
Department of Neurology and Clinical Neurophysiology, St. Olav's University Hospital, 7030, Trondheim, Norway. emre.yaksi@ntnu.no.

Abstract

Brain activity and connectivity alter drastically during epileptic seizures. The brain networks shift from a balanced resting state to a hyperactive and hypersynchronous state. It is, however, less clear which mechanisms underlie the state transitions. By studying neural and glial activity in zebrafish models of epileptic seizures, we observe striking differences between these networks. During the preictal period, neurons display a small increase in synchronous activity only locally, while the gap-junction-coupled glial network was highly active and strongly synchronized across large distances. The transition from a preictal state to a generalized seizure leads to an abrupt increase in neural activity and connectivity, which is accompanied by a strong alteration in glia-neuron interactions and a massive increase in extracellular glutamate. Optogenetic activation of glia excites nearby neurons through the action of glutamate and gap junctions, emphasizing a potential role for glia-glia and glia-neuron connections in the generation of epileptic seizures.

PMID:
31444362
PMCID:
PMC6707163
DOI:
10.1038/s41467-019-11739-z
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center