Classical theories on absence epilepsy suggest that the bilateral generalized spike-wave discharges (SWDs) characterizing absence epilepsy, are caused by thalamo-cortical oscillations, resulting in a condition in which an abnormally excitable cortex interacts with thalamus and brain stem reticular. Recently, a new theory based on experimental findings in the WAG/Rij rat, a genetic model of absence epilepsy, suggests instead that somatosensory cortex contains a focus that initiates a cascade of events that ultimately leads to the occurrence of the bilateral and generalized SWDs if the state of the thalamo-cortical circuitry is favorable. In this case, the cortical focus could be the dominant factor in initiating paroxysmal oscillations within the corticothalamic loops. In order to confirm these hypothesis, we decided to perform in four different cerebral areas (peri-oral cortex, visual cortex, lateral and ventral thalamus) gene-array analysis for cell signaling pathways involved in spindles generation and propagation, validated subsequently by immunohistochemical procedures. The Oligo GEArray® Rat Signal Transduction Pathway Finder™ Gene-array profiles the expression of 113 genes representative of the 18 signal transduction pathways, such as immediate early genes (egr-1, c-fos, c-jun), genes involved in the cell stress pathway (tcf5, hsp27, hspca, p53) or in NFĸB pathway (icam-1, il1, il2, pecam, vcam1). Although preliminary, these data suggest different genes modulations in the cerebral areas and may provide further evidence of a cortical focus in absence epilepsy.