Cellular neuropathology of absence epilepsy in the neocortex: a population of glial cells rather than neurons is impaired in genetic rat model

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 of 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.