Medium-voltage 5–9-Hz oscillations give rise to spike-and-wave discharges in a genetic model of absence epilepsy: in vivo dual extracellular recording of thalamic relay and reticular neurons
Section snippets
Experimental procedures
Fifty-seven adult male Wistar rats weighing 280–350 g were used in this study, which included 31 GAERS (from the 39th to 45th generations) and 26 NE rats (from the 31st to 39th generations). The rats were born and raised under standard conditions in our research unit (INSERM U398, Strasbourg, France). All surgical and animal care procedures adhered to the Guidelines for the Use of Animals in Neuroscience Research (1991) and were approved by our national authorities. All efforts were made to
ECoG in undrugged, behaving GAERS and non-epileptic rats
During wakefulness in GAERS rats, most of the spontaneous SWd (SW complexes at about 6–8 Hz) emerged from short episodes (0.5–3 s) of medium-voltage 5–9-Hz oscillations on a background of low-voltage desynchronized ECoG (Fig. 1). Identical short-lasting (1–3 s) bursts of 5–9-Hz oscillations, which were sometimes accompanied by small-amplitude (<0.5 mV) negative spike components, were also recorded during interictal episodes. Such 5–9-Hz oscillation bursts, which were often characterized by
Discussion
Our results demonstrate that, in a genetic model of absence epilepsy, SWd evolve in the TC system from medium-voltage 5–9-Hz (mean=6 Hz) oscillations, which are fairly distinguishable from sleep spindles. Employing dual extracellular recordings, we further show that reticular cells fire in the burst mode almost always before relay neurons during 5–9-Hz oscillations, which often herald the initial stage of the SWd generation. The frequency of occurrence of the SW complexes (mean=6 Hz)
Conclusion
SWd evolve from medium-voltage 5–9-Hz oscillations in the TC system in a genetic model of absence epilepsy. This rhythm is not itself sufficient to initiate SWd, meaning that genetic factors render TC networks prone to generate epileptic electrical activity, possibly by decreasing the excitability threshold in reticular cells. While these GABAergic neurons play a key role in the synchronization of relay neurons during seizures, glutamatergic TC cells might significantly participate in the
Acknowledgements
We are grateful to John W. Crabtree and Martin Deschênes for comments made on a previous version of the manuscript, and Any Boehrer for selecting the epileptic and non-epileptic strains and for her excellent care of the animals. The Institut Fédératif de Recherche en Neuroscience Strasbourgeois is gratefully acknowledged for providing common services. This research was supported by the Clinique Neurologique, the Faculté de Médecine, the Fondation Française pour la Recherche sur l’Epilepsie, the
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