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Ex vivo MR microimaging of neuronal damage after kainate‐induced status epilepticus in rat: Correlation with quantitative histology
Author(s) -
Pirttilä TiinaRiikka M.,
Pitkänen Asla,
Tuunanen Jarkko,
Kauppinen Risto A.
Publication year - 2001
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1281
Subject(s) - status epilepticus , kainic acid , gliosis , entorhinal cortex , pathology , hippocampus , piriform cortex , histology , kainate receptor , cytoarchitecture , in vivo , biology , medicine , anatomy , neuroscience , glutamate receptor , epilepsy , receptor , microbiology and biotechnology , ampa receptor
The present study was designed to investigate whether T 2 ‐weighted signal changes obtained by microimaging of paraformaldehyde‐fixed brain correlate with the histologically quantified damage in a model of status epilepticus (SE) induced by kainic acid in the rat. Animals were killed at several time points up to 8 weeks after a single intraperitoneal kainate (KA) injection (9 mg/kg). Perfusion‐fixed brains were embedded in gelatin for MR microimaging at 9.4T. After the MRI analysis, the gelatin was removed and the brains were cryoprotected and processed for quantitative histology. Severity of neuronal damage and gliosis were assessed from thionin‐stained serial sections. Correlative analysis of microimaging and histology data was done in the hippocampus, amygdala, parietal rhinal cortex (PaRH), piriform cortex (Pir), and entorhinal cortex. The relative signal intensities in T 2 ‐weighted images correlate with the severity of neuronal damage in the matched histological sections (correlation coefficients of 0.752–0.826). Our data show that MR microimaging ex vivo detects the degree of neuronal damage and its anatomical distribution after KA‐induced SE, thus providing a useful tool for detecting the dynamics of progressive neuronal damage after prolonged seizures. Magn Reson Med 46:946–954, 2001. © 2001 Wiley‐Liss, Inc.