Abstract
In the WAG/Rij rat strain, a genetic model of absence epilepsy, generalized spike-wave discharges (SWDs) are initiated in a specific area of the somatosensory cortex and quickly spread over the cortex and thalamus. This cortical focus regarded as a "leading" spot, driving SWDs (Meeren et al., J. Neurosci., 22, 1480-1495, 2002). A hypothesis that deactivation of the "leading" spot would decrease expression of SWDs was examined using intracortical microinjections of the local anesthetic lidocaine. Lidocaine (1?l of 2%) was unilaterally injected into the somatosensory cortex containing the "leading" spot in 13 WAG/Rij rats, saline was used as control injection. EEG activity was recorded in the area adjacent to the injected site, occipital and bilateral frontal cortices in freely moving animals for two hours after the injection. Application of lidocaine caused (1) reduction of spectral amplitude of EEG in the surrounding area, suggesting local cortical deactivation; (2) reversible decrease in number of SWDs, gradually restored within the second hour after injection. These results show that manipulations in the somatosensory cortex containing the presumptive driving source of SWDs depresses the expression of SWDs. Our findings confirmed the essential role of somatosensory cortex in generalized absence epilepsy, supporting the hypothesis that SWDs may have a local cortical origin.
