Abstracts

RATIONALE: Photochemically-induced thrombosis and brain infarction resulted in large cortical infarcts and recurrent behavioral seizures in adult F344 rats (Kelly et al., Epilepsia 1998;39,Suppl6,29). In other studies, these lesions produced both slow wave and spike and wave discharges in the penumbral area of the infarct zone (Kelly et al., Soc Neurosci Abs, submitted). The hypothesis that these penumbral area discharges were associated with an underlying change in the number or distribution of calcium channels was tested by examining the immunoreactivity of selected glutamate receptor and voltage-gated calcium channel subunits. METHODS: Coronal sections of F344 rat brains were stained by immunohistochemical techniques 24 hr after photothrombosis and after the development of behavioral seizures to assess NMDAR1, GluR1-3, and voltage-gated calcium channel ?1A-D subunit expression. Staining of ipsilateral cortex proximal to the infarct zone was compared qualitatively with that of the homotopic area. RESULTS: GluR2/3 and NMDAR1 immunostaining was reduced in ipsilateral cortex 24 hr after photothrombosis. GluR2/3 immunostaining remained reduced after the onset of behavioral seizures. No change was seen in GluR1 or voltage-gated calcium channel ?1A-D subunits. CONCLUSIONS: Seizure activity in F344 rats following photothrombotic brain infarction may be related to altered glutamate receptor subunit expression in ipsilateral cortex.