Bioenergetic mechanisms of seizure control
- 1Institut für Neurophysiologie, Charité Universitätsmedizin Berlin, Germany
- 2Departement of Medical Neuroscience, Faculty of Medicine, Dalhousie University, Canada
- 3Institute of Physiology (ASCR), Czechia
- 4Departments of Physiology and Cell Biology, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Israel
- 5Institut für Biochemie, Charité Universitätsmedizin Berlin, Germany
Epilepsy is characterized by the regular occurrence of seizures, which follow a stereotypical sequence of alterations in the electroencephalogram. Seizures are typically a self limiting phenomenon, concluding finally in the cessation of hypersynchronous activity and followed by a state of decreased neuronal excitability which might underlie the cognitive and psychological symptoms the patients experience in the wake of seizures. Many efforts have been devoted to understand how seizures spontaneously stop in hope to exploit this knowledge in anticonvulsant or neuroprotective therapies. Besides the alterations in ion-channels, transmitters and neuromodulators, the successive build up of disturbances in energy metabolism have been suggested as a mechanism for seizure termination. Energy metabolism and substrate supply of the brain are tightly regulated by different mechanisms united under the terms neurometabolic and neurovascular coupling. In the current review we summarize the current knowledge whether these mechanisms are sufficient to cover the energy demand of hypersynchronous activity and whether a mismatch between energy need and supply could contribute to seizure termination.
Keywords: seizure, Lactate, neurovascular coupling, neurometabolic coupling, pericyte, CMRO2
Received: 15 Jun 2018;
Accepted: 12 Sep 2018.
Edited by:Li-Rong Shao, School of Medicine, Johns Hopkins University, United States
Reviewed by:Fahmeed Hyder, Yale University, United States
Eva M. Jimenez-Mateos, Royal College of Surgeons in Ireland, Ireland
Hongtao Ma, Weill Cornell Medicine, Cornell University, United States
Copyright: © 2018 Kovacs, Gerevich, Friedman, Otahal, Gabriel, Prager and Berndt. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Richard Kovacs, Institut für Neurophysiologie, Charité Universitätsmedizin Berlin, Berlin, 10117, Berlin, Germany, email@example.com