It is well accepted that absence epilepsy is not accompanied by structural brain abnormalities. In the present report, we challenged this view based on microscopic analysis of neocortex in a genetic model of absence epilepsy, WAG/Rij rats. Density of neurons and glial cells was measured in the motor, somatosensory and cingular cortical areas in epileptic WAG/Rij rats and in non-epileptic control ACI rats. More extensive and significant differences between two strains were found in a population

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... f glial cells and less significant - in neurons. In contract to ACI rats, WAG/Rij rats showed (1) a deficit of glial cells and a lower glia-neuron index in the somatosensory and cingulate areas (deep layers); (2) a reduced number of neurons locally in the motor cortex. The somatosensory cortex (deep layers) is known to play a key role in triggering of epileptic discharges, and an impairment of glia-neuron interactions in this area might underlie pathological processes in a primary epileptic focus. In the motor cortex, epileptiform activity is known to reach the highest amplitude, and this may cause or result from a deficit of neurons. Our data suggest the critical role of glial cells and glia-neuron interactions in pathogenesis of absence epilepsy.