FDG-PET and NeuN-GFAP immunohistochemistry of hippocampus at different phases of the pilocarpine model of temporal lobe epilepsy.

Abstract

Purpose: Hippocampal glucose hypometabolism has been implicated in the pathogenesis of temporal lobe epilepsy (TLE). However, the underlying pathophysiological basis for this hypometabolism remains elusive. The aim of this study was to investigate the relationship between hippocampal hypometabolism and the histological changes seen in rats after systemic pilocarpine treatment.Methods: 18F-fluorodeoxyglucose (FDG) small-animal positron emission tomography (microPET) was performed on day zero (untreated), day seven (latent) and day sixty (chronic phase) after the initial status epilepticus. The microPET imaging data were correlated with the immunoreactivity of neuron-specific nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) in the hippocampus at each time point.Results: 18F-FDG-microPET images showed the hippocampus presented with persistent hypometabolism during epileptogenesis and partly recovered in the chronic phase. Hippocampal glucose uptake defects correlate with NeuN immunoreactivity in the latent phase and GFAP immunoreactivity in the chronic phase.Conclusions: Severe glucose hypometabolism in the hippocampus during the latent phase correlates with neuronal cell loss. The partial recovery of hippocampal glucose uptake in the chronic phase may be due to astrogliosis.