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Abstract
In rats, this study determined the impact of systemic hypoxia during late kainate-induced
status epilepticus on hippocampal neuron loss and mossy fiber sprouting. Non-fasted
Sprague Dawley rats were prepared as follows: Naive controls (n=5); rats placed 2
min in a hypoxia chamber (hypoxia only; n=6); rats that seized for more than 6 h from
kainic acid (KA-status; 12 mg/kg; i.p.; n=7); and another KA-status group placed into
the hypoxia chamber 75 min after the convulsions started (KA-status/hypoxia; n=16).
All rats, except for half of the KA-status/hypoxia animals, were perfused 2 weeks
later (short-term). The other 8 KA-status/hypoxia rats were perfused after 2 months
(long-term). Hippocampal sections were studied for neuron densities and aberrant mossy
fiber sprouting at three ventral to dorsal levels. Fascia dentata (FD) mossy fiber
sprouting was quantified as an increase in the inner minus outer molecular layer (IML-OML)
gray value (GV) difference. Behaviorally, KA-status/hypoxia rats had a shorter duration
of convulsive status epilepticus than KA-status animals without anoxia. Hippocampal
sections showed that compared to controls: (1) hypoxia-only rats showed no differences
in ventral neuron densities and neo-Timm's stained IML-OML GVs; (2) KA-status rats
had decreased CA3 densities and a non-significant increase in ventral IML-OML GV differences;
and (3) KA-status/hypoxia short-term animals showed decreased hilar, CA3 and CA1 densities
and increased ventral IML-OML GV differences. Compared to KA-status/hypoxia short-term
rats, long-term animals showed no differences in ventral hippocampal neuron densities,
but middle and dorsal sections demonstrated increased IML-OML GV differences and animals
were observed to have spontaneous limbic epilepsy. These results indicate that rats
exposed to kainate-induced status epilepticus for over 1 h and then a hypoxic insult
had a shorter duration of convulsive status, decreased hippocampal neuron densities
and greater FD mossy fiber sprouting than controls and the amount of neuronal damage
and sprouting was slightly more than animals subjected to 6 h of kainate-induced status.
This supports the hypothesis that a physiologic insult during status can shorten the
convulsive episode, but still produce hippocampal pathology with a number of clinical
and pathologic similarities to human mesial temporal lobe epilepsy (MTLE).