Hippocamus neuroplasticity in immature rats following recurrent seizure injury

Objectives To observe histopathological changes thus understanding the neuroplasticity in immature rat hippocampus following recurrent seizure injury. Methods Rats at postnatal day 10 (n = 48) were divided into 2 groups: the control group (n = 18) treated daily with normal salinefor 5 consecutive days, and experimental group (n = 30) treated with daily administration of pentylenetetrazol (PTE) for 5 consecutive days to induce recurrent convulsions. The neurons in dentate granule area, CA1, CA3, as well as in hilar were stained with thionin and counted to study the profile of necrosis and apoptosis. Timm' s method of silver sulfide staining was adopted to observe the mossy fiber sprouting two weeks after the last spell of seizures. Expression of NF-κB was examined by immunohistochemistry at 24 hours after the last spell of seizures. Results Cell counting of CA1, CA3 and hilar neurons demonstrated no differences from that of the controls (P 0.05), whereas neurons in dentate granule increased significantly with comparison to control (23.25±3.06 vs 16.25±1.58, P 0.05) . More expression of NF-κB was observed in CA1, CA3 and dentate granule cells 24 hours later after PTZ-kindling than that of the controls (P 0.05) . The mossy fiber sprouting in the CA, was significantly increased in the neonatal rats in experimental group comparing with that of the controls (1.50±0.92 vs 0.25±0.46, P 0.01) . Conclusions No cell loss was seen in hippocampus of neonatal rats after recurrent kindling. The high expression of NF-κB could be putatively one of the important molecular bases underlying the special resistance of the neurons in premature brain to the epileptic cerebral lesions. Neurons of dentate granule increased significantly after recurrent seizures, which seemed to be the initial mechanism for mossy fiber sprouting in immature rats.