Increased hippocampal T2 in a rat model of pentylenetetrazol-induced kindling correlates with seizure scores

BackgroundClinical and experimental magnetic resonance imaging (MRI) studies have demonstrated that epilepsy is associated with hippocampal atrophy and T2-related abnormalities. The main aim of the present study is to investigate the mechanisms underlying regional T2 changes in a rat model of pentylenetetrazol (PTZ)-kindling.MethodsSprague-Dawley rats received 14 doses of PTZ or saline every second day, and their convulsant responses to each PTZ injection were scored. The animals were imaged 7–10 days after the final dose. Based on their seizure scores during treatment and in a screening test performed 2 weeks post-treatment, the PTZ-treated animals were retrospectively divided into the kindled group and the unkindled group. Selected animals were sacrificed for histology after the screening test.ResultsStarting from the 8th injection, the average seizure score in kindled animals became significantly higher than that in unkindled animals. About half of the PTZ-treated rats developed hippocampal atrophy. Whether kindled or not, treated animals showed selective neuronal loss and astrocytosis in the hippocampus. No significant T2 changes were observed for the unkindled rats, but T2 was significantly elevated in the hippocampus and entorhinal cortex of the kindled animals. T2 in the hippocampus and entorhinal cortex of the treated animals correlated positively with the sum of the seizure scores over the entire kindling period.ConclusionsInstead of being merely a manifestation of neuronal degeneration, T2 increases in the hippocampus and EC of the PTZ-kindled animals may have reflected neurobiologic processes that are related to kindling epileptogenesis.