2006Zhonghua xingwei yixue yu naokexue zazhiRequires access

Dynamic change of neuronal apoptosis of hippocampus in rats following kainic acid-induced seizures

Shi Zhi-yong

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Abstract

Objective To investigate the change of neuronal morphology and apoptosis in hippocampus by kainic acid(KA) induced status epilepsy(SE) in rats, and the neuroprotective effect of anti-epilepsy drug. Methods 90 Wistar rats were classified as control group, KA group and carbamazepine (CBZ) group. The posterior two groups were also divided into 6 sub-groups (1 h, 4 h, 12 h, 24 h, 48 h and 72 h) according to seizure attack at the different time point. To observe the change of ethology after seizure attack, the change of neuronal morphology of CA1 and CA3 sectors within the hippocampus with the Hematoxylin and Eosin(HE) stain and the neuronal apoptosis with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL stain). Results The rats appeared severe seizures after injecting KA, there were sporadic positive cells (CA1 sector KA group 6.53±1.36, CBZ group 5.85±1.68. CA3 sector:KA group 9.58±1.63, CBZ group 7.36±1.27) in CA1 and CA3 sectors within the hippocampus at 12 h after seizure attack, the numbers of positive cells of CA1 and CA3 sectors significantly increased at 48 h post- KA treatment (P0.01) (CA1 sector:KA group 42.263± 3.28,CBZ group 35.39±2.36.CA3 sector:KA group 57.64±12.76, and CBZ group 38.37±13.65). The numbers of positive cells obviously decreased by intervention with CBZ (P0.05). Conclusion The delayed neuronal death after KA induced SE was possibly caused by apoptosis, and CBZ can inhibit neuronal apoptosis of hippocampus at SE.

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Objective To investigate the change of neuronal morphology and apoptosis in hippocampus by kainic acid(KA) induced status epilepsy(SE) in rats, and the neuroprotective effect of anti-epilepsy drug. Methods 90 Wistar rats were classified as control group, KA group and carbamazepine (CBZ) group. The posterior two groups were also divided into 6 sub-groups (1 h, 4 h, 12 h, 24 h, 48 h and 72 h) according to seizure attack at the different time point. To observe the change of ethology after seizure attack, the change of neuronal morphology of CA1 and CA3 sectors within the hippocampus with the Hematoxylin and Eosin(HE) stain and the neuronal apoptosis with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL stain). Results The rats appeared severe seizures after injecting KA, there were sporadic positive cells (CA1 sector KA group 6.53±1.36, CBZ group 5.85±1.68. CA3 sector:KA group 9.58±1.63, CBZ group 7.36±1.27) in CA1 and CA3 sectors within the hippocampus at 12 h after seizure attack, the numbers of positive cells of CA1 and CA3 sectors significantly increased at 48 h post- KA treatment (P0.01) (CA1 sector:KA group 42.263± 3.28,CBZ group 35.39±2.36.CA3 sector:KA group 57.64±12.76, and CBZ group 38.37±13.65). The numbers of positive cells obviously decreased by intervention with CBZ (P0.05). Conclusion The delayed neuronal death after KA induced SE was possibly caused by apoptosis, and CBZ can inhibit neuronal apoptosis of hippocampus at SE.

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Available abstract

Objective To investigate the change of neuronal morphology and apoptosis in hippocampus by kainic acid(KA) induced status epilepsy(SE) in rats, and the neuroprotective effect of anti-epilepsy drug. Methods 90 Wistar rats were classified as control group, KA group and carbamazepine (CBZ) group. The posterior two groups were also divided into 6 sub-groups (1 h, 4 h, 12 h, 24 h, 48 h and 72 h) according to seizure attack at the different time point. To observe the change of ethology after seizure attack, the change of neuronal morphology of CA1 and CA3 sectors within the hippocampus with the Hematoxylin and Eosin(HE) stain and the neuronal apoptosis with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL stain). Results The rats appeared severe seizures after injecting KA, there were sporadic positive cells (CA1 sector KA group 6.53±1.36, CBZ group 5.85±1.68. CA3 sector:KA group 9.58±1.63, CBZ group 7.36±1.27) in CA1 and CA3 sectors within the hippocampus at 12 h after seizure attack, the numbers of positive cells of CA1 and CA3 sectors significantly increased at 48 h post- KA treatment (P0.01) (CA1 sector:KA group 42.263± 3.28,CBZ group 35.39±2.36.CA3 sector:KA group 57.64±12.76, and CBZ group 38.37±13.65). The numbers of positive cells obviously decreased by intervention with CBZ (P0.05). Conclusion The delayed neuronal death after KA induced SE was possibly caused by apoptosis, and CBZ can inhibit neuronal apoptosis of hippocampus at SE.

Key concepts: Kainic acid, TUNEL assay, Hippocampus, Epilepsy, Apoptosis, Internal medicine, Endocrinology, Terminal deoxynucleotidyl transferase

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