Absence epilepsy is an epileptic syndrome which main symptom is a transient alteration of consciousness, with generalized spike-and-wave discharges in EEG, which arise from a dysfunction in the corticothalamic loop and are initiated from a subclass of pyramidal neurons located in the deep layers of the somatosensory cortex. I have investigated two unresolved, issues: 1/ the role of the cortical inhibition in the ictogenic processes, 2/ the neurophysiological mechanisms of sensory processing during absence seizures. By the means of EEG and intracellular recordings in vivo in an animal model: the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), I have examined how the early excitation in theictogenic neurons during seizures was shortly followed by a chlore-dependent synaptic hyperpolarization, concomitant with bursting activities in local GABAergic interneurons. The GABA system has an active inhibitory effect, which constraints the firing of ictogenic neurons within a tight temporal window. In a second study, in human and GAERS, I explored how sensory information was processed during SWDs. In the epileptic child, visual stimulations resulted in occipital evoked potentials, bigger than in non-epileptic subjects. Tactile stimulation of the GAERS applied during seizures induced cortical evoked potentials, reflected in the pyramidal neurons by excitatory synaptic potentials bigger than in interictal condition. Impairment of consciousness during absences do not result from a filtering of sensory information. These researches provide new information on the functional properties of the cortical circuits expressing the electrical paroxysms during absence seizures
