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J Physiol Volume 509, Number 2, 449-456, June 1, 1998
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The Journal of Physiology (1998), 509.2, pp. 449-456
© Copyright 1998 The Physiological Society

Intracellular recordings in thalamic neurones during spontaneous spike and wave discharges in rats with absence epilepsy

Didier Pinault, Nathalie Leresche *, Stéphane Charpier ¹, Jean-Michel Deniau ¹, Christian Marescaux, Marguerite Vergnes and Vincenzo Crunelli ²

INSERM U398, Faculté de Médecine, 11 rue Humann, 67085 Strasbourg, France * Département de Neurobiologie Cellulaire and ¹ Neurochimie-Anatomie, Institut des Neurosciences, Université Pierre et Marie Curie, 9 quai Saint-Bernard, F-75005 Paris, France and ² Physiology Unit, School of Molecular and Medical Biosciences, University of Wales Cardiff, Cardiff, UK

  1. In vivo extracellular and intracellular recordings were performed from thalamocortical (TC) neurones in a genetic model of absence epilepsy (genetic absence epilepsy rats from Strasbourg) during spontaneous spike and wave discharges (SWDs).

  2. Extracellularly recorded single units (n = 14) fired either a single action potential or a high frequency burst of up to three action potentials, concomitantly with the spike component of the spike-wave complex.

  3. Three main events characterized the intracellular activity of twenty-six out of twenty-eight TC neurones during SWDs: a small amplitude tonic hyperpolarization that was present throughout the SWD, rhythmic sequences of EPSP/IPSPs occurring concomitantly with the spike-wave complexes, and a small tonic depolarization at the end of the SWD. The rhythmic IPSPs, but not the tonic hyperpolarization, were mediated by activation of GABAA receptors since they reversed in polarity at -68 mV and appeared as depolarizing events when recording with KCl-filled electrodes.

  4. The intracellular activity of the remaining two TC neurones consisted of rhythmic low threshold Ca2+ potentials, with a few EPSP/IPSP sequences present at the start of the SWD.

  5. These results obtained in a well-established genetic model of absence epilepsy do not support the hypothesis that the intracellular activity of TC neurones during SWDs involves rhythmic sequences of GABAB IPSPs and low threshold Ca2+ potentials.




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