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. 2008 Jun;10(3):367-70.

[Effect of extracts of Ginkgo biloba leaf on learning-memory ability and NMDA receptor 1 expression in the hippocampus in rats with kindling-induced epilepsy]

[Article in Chinese]
Affiliations
  • PMID: 18554470

[Effect of extracts of Ginkgo biloba leaf on learning-memory ability and NMDA receptor 1 expression in the hippocampus in rats with kindling-induced epilepsy]

[Article in Chinese]
Fang-Rong Duan et al. Zhongguo Dang Dai Er Ke Za Zhi. 2008 Jun.

Abstract

Objective: To study the effect of extracts of Ginkgo biloba leaf (EGb), a catalyzer of central nervous system, on learning-memory ability and possible mechanism in rats with kindling-induced epilepsy.

Methods: Forty postnatal day 21 (P21) and 40 postnatal day 35 (P35) Sprague-Dawley (SD) rats were randomly respectively assigned to five groups: normal sodium (NS) control, kindling epilepsy model, high, middle and low dosage of EGb-treated kindling epilepsy. The kindling epilepsy model was established by an intraperitoneal injection of pentetrazole (PTZ). The learning-memory ability and NMDA receptor 1 (NMDAR1) expression in the hippocampus were measured by Y-maze test and immunohistochemistry assay respectively.

Results: The stimulation times for reaching to academic standard in the Y-maze test in the two ages PTZ kindling groups was significantly more than that in the corresponding NS control groups (P<0.01). After EGb treatment the achievement of the Y-maze test in the three treatment groups was significantly improved in a dose-dependent manner, the higher the dosage, the better the achievement (P<0.01). Immunohistochemistry assay showed that the expression of NMDAR1 in the two ages PTZ kindling groups was significantly higher than that in the corresponding NS control groups (P<0.01). Compared with the corresponding untreated kindling model groups, the expression of NMDAR1 in the two ages EGb treatment groups was significantly reduced in a dose-dependent manner (P<0.01).

Conclusions: EGb can improve learning-memory ability in epileptic rats at different developmental phases in a dose-dependent manner, possibly through a reduction of NMDAR1 expression in the hippocampus.

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