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Next Article 
Journal of Neuroscience, Vol 15, 6301-6313, Copyright © 1995 by Society for Neuroscience
Preferential neuronal loss in layer III of the medial entorhinal cortex in rat models of temporal lobe epilepsy
F Du, T Eid, EW Lothman, C Kohler and R Schwarcz
Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore 21228, USA.
We recently described a pronounced neuronal loss in layer III of the
entorhinal cortex (EC) in patients with intractable temporal lobe epilepsy
(Du et al., 1993a). To explore the pathophysiology underlying this distinct
neuropathology, we examined the EC in three established rat models of
epilepsy using Nissl staining and parvalbumin immunohistochemistry. Adult
male rats were either electrically stimulated in the ventral hippocampus
for 90 min or injected with kainic acid or lithium/pilocarpine. Animals
were observed for behavioral changes for up to 6 hr and were killed 24 hr
or 4 weeks after the experimental treatments. At 24 hr, all animals that
had exhibited a bout of acute status epilepticus showed a consistent
pattern of neuronal loss in the EC in Nissl-stained sections.
Neurodegeneration was most pronounced in layer III of the medial Ec at all
dorsoventral levels. A few surviving neurons were frequently present in the
lesioned area. An identical pattern of nerve cell loss was also seen in the
EC of rats killed 4 weeks following the treatments. This lesion was
completely prevented by an injection of diazepam and pentobarbital, given 1
hr after kainic acid administration. Immunohistochemistry demonstrated a
relative resistance of parvalbumin-positive neurons in layer III of the
medial EC. Taken together, these experiments indicate that prolonged
seizures cause a preferential neuronal loss in layer III of the medial EC
and that this lesion may be related to a pathological elevation of
intracellular calcium ion concentrations.
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