Abstracts

Rationale: There are many types of epilepsy, and we need to know the similarity and the differences to choose the appropriate treatment depending on the pathology. The various types of epileptic animal models had been developed. Therefore we tried to visualize the differences between two epileptic animal models using positron emission tomography (PET) focusing on brain metabolism and neuroinflammation. Methods: We compare 2 epileptic animal models which are considered as temporal lobe epilepsy model, EL mice which is genetic epileptic model mice showing general seizures induced by postural stimulation with aging, and status epileptic (SE) model rat which can have spontaneous seizures after SE induced by pilocarpine intraperitoneal injection. EL mice is an idiopathic epileptic model and pilocarpine SE rat is a symptomatic epileptic model. We conducted PET imaging using [18F]FDG, [11C]1-methyl-L-tryptophan(1MT), radiolabeled tryptophan, and [11C]Ac5216, radiolabeled 18kDa Translocator protein (TSPO). Additionally, we analyzed brain inflammation and neuronal loss immunohistologically. Results: In EL mice, the uptake of [18F]FDG in whole brain was significantly decreased than ddY mice which is a maternal line of EL mice without seizures. The uptake of [11C]1MT in whole brain was significantly increased than ddY mice from 5weeks of age without seizures to 6 months of age. The uptake of [11C]Ac5216 was significantly higher in the stratium of EL mice, however the rest of the brain doesn't show significant difference. Pilocarpine SE rats also showed low uptake of [18F]FDG, however [11C]1MT uptake wasn't different between SE rats, non-SE rats and saline-injected control group of rats. The uptake of [11C]Ac5216 was higher in SE rat compared to non-SE rats and control rats. In immunohistochemical analysis, the number of astrocytes in the EL mouse cortex was significantly increased than ddY mouse. The neuronal loss and microglial activation were not evident in EL mouse brain. In pilocarpine SE rat brain, the neuronal loss and microglial activation in the hippocampus and amygdala was significant than control rat brain. Conclusions: There is a difference of brain metabolism and neuronal inflammation between two animal models considered as temporal lobe epilepsy. PET imaging is possibly a powerful modality for diagnosing and subtyping epilepsy on the mechanistic basis. Funding: No funding