Abstracts

Genetic Absence Epilepsy Rats of Strasbourg (GAERS) are a well-validated model of absence epilepsy. Like the human condition, the nature of the underlying defect resulting in the epileptic phenotype in GAERS is still unknown, but the inhibitory neurotransmitter GABA has been implicated and neuropeptide Y (NPY) may be important. We investigated whether there was a regional localization of specific GABA receptor subtypes or NPY in brain structures involved in generating epileptiform activity in GAERS vs. non-epileptic control (NEC) rats. Male GAERS and NECs were given a 30-minute EEG recording to verify animal phenotype. Regional localization of NPY and GABA receptor subtypes; GABA[sub]A[/sub] gamma[sub]2[/sub], GABA[sub]A[/sub] alpha2 and GABA[sub]B[/sub] was compared in brain sections of GAERS (n=7) vs. NECs (n=6) using immunohistochemistry. Staining was graded by a blinded observer on a scale of 0-4 for the following brain regions important in thalmocortical circuitry: reticular thalamus, ventrobasal thalamus, centromedial thalamus, inferomedial thalamus, superomedial thalamus, dorsal thalamus, and somatosensory cortex. Moderate to high levels (Grade 2-4) of neuronal staining was seen in all thalamocortical areas examined for all GABA receptor subtypes and for NPY. However, no significant differences were found between GAERS and NECs in staining for the GABA receptor subtypes or for NPY for any of the brain regions examined (all p[gt]0.05). The demonstrated lack of difference in the topographic pattern of staining for GABA receptor subtypes or NPY between GAERS and NEC rats, suggests that alterations in their expression is unlikely to be a major contributor to the epileptic phenotype of GAERS. (GABA receptor antibodies were a gift of Professor W Sieghart, University of Vienna, Austria)