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Brain. 2017 Sep 1;140(9):2355-2369. doi: 10.1093/brain/awx179.

Involvement of fast-spiking cells in ictal sequences during spontaneous seizures in rats with chronic temporal lobe epilepsy.

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Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, 4401 University Dr W, Lethbridge, AB, T1K 3M4, Canada.
Department of Neurology, Ghent University, Gent, Belgium.
Neuro-Electronics Research Flanders, Leuven, Belgium.
VIB, Leuven, Belgium.
Brain and Cognition Research unit, KU Leuven, Leuven, Belgium.
Department of Neurosurgery, and Stanford Neurosciences Institute, Stanford University, Stanford, CA, USA.
Department of Neurobiology and Behavior, University of California at Irvine, Center for the Neurobiology of Learning and Memory, Irvine, CA, USA.


See Lenck-Santini (doi:10.1093/awx205) for a scientific commentary on this article. Epileptic seizures represent altered neuronal network dynamics, but the temporal evolution and cellular substrates of the neuronal activity patterns associated with spontaneous seizures are not fully understood. We used simultaneous recordings from multiple neurons in the hippocampus and neocortex of rats with chronic temporal lobe epilepsy to demonstrate that subsets of cells discharge in a highly stereotypical sequential pattern during ictal events, and that these stereotypical patterns were reproducible across consecutive seizures. In contrast to the canonical view that principal cell discharges dominate ictal events, the ictal sequences were predominantly composed of fast-spiking, putative inhibitory neurons, which displayed unusually strong coupling to local field potential even before seizures. The temporal evolution of activity was characterized by unique dynamics where the most correlated neuronal pairs before seizure onset displayed the largest increases in correlation strength during the seizures. These results demonstrate the selective involvement of fast spiking interneurons in structured temporal sequences during spontaneous ictal events in hippocampal and neocortical circuits in experimental models of chronic temporal lobe epilepsy.


neuronal population activity, GABAergic cells; temporal lobe epilepsy

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