2006Di-san junyi daxue xuebaoRequires access

Effect of estrogen on astrocyte and synaptic plasticity in hippocampus of PTZ kindling rat model of epilepsy

Zhong Yang

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Abstract

Objective To investigate the effect of estrogen on gliosis, synaptic proliferation and reorganization in hippocampus of rats with chronic epilepsy induced by pentylenetetrazol (PTZ). Methods Thirty-two Wistar rats were randomly divided into normal control group, PTZ kindling epilepsy group, estrogen+PTZ group and estrogen +Tamoxifen (mixed estrogen antagonist)+PTZ group. The PTZ kindling epilepsy group was intraperitoneally injected with 35 mg/kg PTZ once a day, then the behavior of the rats in one hour was observed. The estrogen interfered group was intramuscluarly injected of 0.6 μg/kg β-estradiol 6 h before PTZ injection, 1/3 d. The estrogen+Tamoxifen interfered group was injected of Tamoxifen into lateral cerebral ventricle 1 h before estrogen injection. If the severe epileptic seizures occurred three times, the rats were ready for detecting the expression of filial fibrillary acidic protein (GFAP) and synaptophysin (P38) by immunohistochemical technique. Results Epileptic seizure occoured earlier and more severely in most rats of estrogen interfered group than no estrogen interfered group. Rats in all model groups were found more astrocyte proliferation and positive synaptophysin staining, especially in the CA2, CA3 and hilar areas of dentate gyrus (DG) of hippocampus than control group. Estrogen+Tamoxifen interfered group showed significant difference as compared with other groups (P0.01). Conclusion The changes in the GFAP and synaptic proliferation in the hippocampus after PTZ injection are probably related to the formation of abnormal discharge circuit, and finally lead to the seizures in rats. Estrogen can enhance the seizure and the alteration in rat hippocampus, but tamo-xifen plays the opposite role. Estrogen is involved in the gliosis, synaptic proliferation and reorganization of the mechanism of chronic epilepsy.

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Objective To investigate the effect of estrogen on gliosis, synaptic proliferation and reorganization in hippocampus of rats with chronic epilepsy induced by pentylenetetrazol (PTZ). Methods Thirty-two Wistar rats were randomly divided into normal control group, PTZ kindling epilepsy group, estrogen+PTZ group and estrogen +Tamoxifen (mixed estrogen antagonist)+PTZ group. The PTZ kindling epilepsy group was intraperitoneally injected with 35 mg/kg PTZ once a day, then the behavior of the rats in one hour was observed. The estrogen interfered group was intramuscluarly injected of 0.6 μg/kg β-estradiol 6 h before PTZ injection, 1/3 d. The estrogen+Tamoxifen interfered group was injected of Tamoxifen into lateral cerebral ventricle 1 h before estrogen injection. If the severe epileptic seizures occurred three times, the rats were ready for detecting the expression of filial fibrillary acidic protein (GFAP) and synaptophysin (P38) by immunohistochemical technique. Results Epileptic seizure occoured earlier and more severely in most rats of estrogen interfered group than no estrogen interfered group. Rats in all model groups were found more astrocyte proliferation and positive synaptophysin staining, especially in the CA2, CA3 and hilar areas of dentate gyrus (DG) of hippocampus than control group. Estrogen+Tamoxifen interfered group showed significant difference as compared with other groups (P0.01). Conclusion The changes in the GFAP and synaptic proliferation in the hippocampus after PTZ injection are probably related to the formation of abnormal discharge circuit, and finally lead to the seizures in rats. Estrogen can enhance the seizure and the alteration in rat hippocampus, but tamo-xifen plays the opposite role. Estrogen is involved in the gliosis, synaptic proliferation and reorganization of the mechanism of chronic epilepsy.

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Available abstract

Objective To investigate the effect of estrogen on gliosis, synaptic proliferation and reorganization in hippocampus of rats with chronic epilepsy induced by pentylenetetrazol (PTZ). Methods Thirty-two Wistar rats were randomly divided into normal control group, PTZ kindling epilepsy group, estrogen+PTZ group and estrogen +Tamoxifen (mixed estrogen antagonist)+PTZ group. The PTZ kindling epilepsy group was intraperitoneally injected with 35 mg/kg PTZ once a day, then the behavior of the rats in one hour was observed. The estrogen interfered group was intramuscluarly injected of 0.6 μg/kg β-estradiol 6 h before PTZ injection, 1/3 d. The estrogen+Tamoxifen interfered group was injected of Tamoxifen into lateral cerebral ventricle 1 h before estrogen injection. If the severe epileptic seizures occurred three times, the rats were ready for detecting the expression of filial fibrillary acidic protein (GFAP) and synaptophysin (P38) by immunohistochemical technique. Results Epileptic seizure occoured earlier and more severely in most rats of estrogen interfered group than no estrogen interfered group. Rats in all model groups were found more astrocyte proliferation and positive synaptophysin staining, especially in the CA2, CA3 and hilar areas of dentate gyrus (DG) of hippocampus than control group. Estrogen+Tamoxifen interfered group showed significant difference as compared with other groups (P0.01). Conclusion The changes in the GFAP and synaptic proliferation in the hippocampus after PTZ injection are probably related to the formation of abnormal discharge circuit, and finally lead to the seizures in rats. Estrogen can enhance the seizure and the alteration in rat hippocampus, but tamo-xifen plays the opposite role. Estrogen is involved in the gliosis, synaptic proliferation and reorganization of the mechanism of chronic epilepsy.

Key concepts: Synaptophysin, Pentylenetetrazol, Kindling, Estrogen, Hippocampus, Dentate gyrus, Epilepsy, Endocrinology

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