Cell swelling precedes seizures induced by inhibition of astrocytic metabolism.
Journal article, 2008

It is currently unknown what processes take place at the interface between non-ictal and ictal activity during seizure initiation. In this study, using paralysed awake rats, we focally inhibited astrocytic metabolism with fluorocitrate (FC), causing seizures. We measured changes in electroencephalogram (EEG) (0-300 Hz), and extracellular ion-concentrations during ictal onsets defining possible relationships with impedance-determined cell swelling. In animals showing ictal activity (69%) there were spike-wave discharges, spike-wave discharges followed by spreading depression and spreading depression without any discharges. In a high proportion of spike-wave discharges (>95%), just prior to the first spike-wave discharge, there was a decrease in the volume of the extracellular space. Following the initiation of cell swelling and prior to discharges, there were increases in high-frequency (150-300 Hz) EEG activity, increases in extracellular potassium- and decreases in extracellular calcium-concentrations. We suggest that EEG and ionic changes are not causative of cell swelling. Cell swelling due to metabolic failure in astrocytes at the injected site may release excitatory amino acids. At the same time, our results suggest ion homeostasis is not maintained and increased neuronal excitability and synchronisation occur. These could be the drivers changing normal brain activity into ictal activity.

Author

Marita Broberg

Flinders University

Kenneth Pope

Flinders University

T Lewis

Flinders University

Torsten Olsson

Chalmers, Signals and Systems, Signalbehandling och medicinsk teknik, Biomedical Signals and Systems

Michael Nilsson

University of Gothenburg

John Willoughby

Flinders University

Epilepsy Research

0920-1211 (ISSN)

Vol. 80 2-3 132-41

Subject Categories

Medical Laboratory and Measurements Technologies

Neurology

Areas of Advance

Life Science Engineering (2010-2018)

DOI

10.1016/j.eplepsyres.2008.03.012

More information

Created

10/8/2017