FEBRILE CONVULSION-INDUCED
BRAIN DAMAGE: A PRELIMINARY LABORATORY STUDY
Chang XZ, Qin J, Wu XR
Peking University First
Hospital, Beijing, China
Objective: To study febrile
convulsion (FC) induced neuronal damage.
Methods: Warm-water-immersion
model was used to study FC-induced neuronal injury, and the long-term
effects of FC on later seizure susceptibility and behavior. One and 15
seizures were induced in SD rats beginning at 22 days of age, then some of
them were left unstimulated for 3 months, and restimulated. Neuronal
apoptosis was examined by TUNEL stain and electron microscopy. Granule cell
sprouting was detected with Timm stain, and memory ability was tested using
a Morris water maze. The effect of FC on the expression of neuronal nitric
oxide synthase (nNOS) was studied immunohistochemically.
Results: Neuronal apoptosis was
obvious after repeated febrile convulsions (FCs). The mitochodrion changes,
manifesting as swelling, ridge unclear or disappeared and vacuolar
appearance, were seen electron-microscopically. Rats with FC performed
significantly worse in the Morris water maze, lasting at least over 3
months. Sprouting of granule cell collaterals into the inner molecular
layer of the dentate was detected in the rats with repeated FCs. The expression
of nNOS was increased in the rats with FC.
Conclusion: Repeated FCs may cause
neuronal damage, and apoptosis may participate in the process. FCs may
result in long-term behavior deficit and increase seizure susceptibility.
Mossy fiber sprouting may underlie the long-term effects of FC, and nitric
oxide (NO) may take a part in the process of neuron injury and memory
damage.