RESUMEN
BACKGROUND: Various neuronal and glial factors which participate in neural differentiation, including neural cell adhesion molecule (NCAM), are upregulated in pathogenesis of temporal lobe epilesy (TLE).This study aimed to investigate hte effect of (R-)-N6-phenylisopropyladenosine (RPIA), an adenosine A1 receptor agonist, on the morphological alteration of NCAM immunoreactivity (IR) in limbic system of Kainic acid (KA)-induced epileptic rats. METHODS: Experiment animals were divided into control group, KA treatment only (10 mg/kg. i.p.)group, and RPIA pretreatment (100 microgram/kg. i,p, 10 min prior to injection of KA) group. Animals were sacrificed at 24 hours and 1 week after KA treatment. Luxol fast blue-cresyl violet stain for histopathological observation, and NCAM immunohistochemistry to study alteration of NCAM IR in limbic system were performed. RESULTS: Neuronal loss in CA1 and CA3areas of hippocampus, piridorm cortex, basolateral amygdala nucleus and lateral dorsal thalamic nucleus were induced by KA unjection, and thoes were reduced by RPIA pretreatment. Inrease of NCAM-IR was observed in interneurons of all hippocampal areas. except CA2 area, pirform cortex and basolateral amygdala nucleus at 24 hours after KA injection. and increased NCAM-IR was observed in cell membrane and processes of neuroglia, dentate granule cells and pyramidal cells in CA1 area of hippocampus. and neurons in piriform cortex, amygdala and lateral dorsal thalamic nucleus 1 week after KA injection, but those changes were milder than those at 24 hours after KA injection. RPIA pretreatment significantly reduced KA-induced NCAM-IR in hippocampal CA3, CA1 area, piriform cortex, amtgdala and lateral dorsal thalamic nucleus. CONCLUSION: We suggest that decrease of NCAM immunoreactivity is associated with neuprotective effects of RPIA on limbic system against KA neurotoxiciy.