Abstract
Previous imaging studies have shown the morphological malformation and the alterations of ionic mobility, water contents, electrical properties, or metabolites in seizure brains. Magnetic resonance electrical properties tomography (MREPT) is a recently developed technique for the measurement of electrical tissue properties with a high frequency that provides cellular information regardless of the cell membrane. In this study, we examined the possibility of MREPT as an applicable technique to detect seizure-induced functional changes in the brain of rats. Ultra-high field (9.4 T) magnetic resonance imaging (MRI) was performed, 2 h, 2 days, and 1 week after the injection of N-methyl-D-aspartate (NMDA; 75 mg/kg). The conductivity images were reconstructed from B1 phase images using a magnetic resonance conductivity imaging (MRCI) toolbox. The high-frequency conductivity was significantly decreased in the hippocampus among various brain regions of NMDA-treated rats. Nissl staining showed shrunken cell bodies and condensed cytoplasm potently at 2 h after NMDA treatment, and neuronal cell loss at all time points in the hippocampus. These results suggest that the reduced electrical conductivity may be associated with seizure-induced neuronal loss in the hippocampus. Magnetic resonance (MR)-based electrical conductivity imaging may be an applicable technique to non-invasively identify brain damage after a seizure.
Highlights
Epilepsy is a neurological disorder characterized by recurrent and long-lasting seizures.A seizure is a paroxysmal symptom induced by abnormally excessive excitatory activity in the brain [1]
Seizures were prominently sustained for 1 h after NMDA treatment, and entirely abolished within 90 min in all of the rats
We investigated the expression of cleaved caspase 3 (CASP3), an apoptotic executor, in the hippocampus of NMDA-treated rats
Summary
A seizure is a paroxysmal symptom induced by abnormally excessive excitatory activity in the brain [1]. Previous studies have reported that seizures occur due to the excessive release of glutamate [2,3]. A microdialysis study for epilepsy patients showed an increased concentration of glutamate in the hippocampus during seizures [4,5]. Rodents treated with glutamate agonists, such as N-methyl-D-aspartate (NMDA) and kainic acid (KA), have been used as seizure animal models, showing tonic–clonic seizures [6,7]. Previous studies have shown that the glutamate agonists induced neuronal cell death in the rodent brains by regulating the cell death-related proteins, such as caspase 3 (CASP3), BCL2, and P38, along with seizures [9,10,11]
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