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目的探讨阳离子-氯离子转运体 NKCC1(内向 Na~+,K~+-2Cl~-协同运输)、KCC2(外向K~+-Cl~-协同运输)mRNA 在皮质发育障碍致痫机制中的作用。方法在 SD 大鼠孕17 d 腹腔内注入卡莫司汀(BCNU)制作皮质发育障碍模型;Nissl 染色观察 P60 d 仔鼠病理变化;P60 d 用逆转录-聚合酶链反应(RT-PCR)方法检测两组雄性仔鼠海马区 NKCC1、KCC2 mRNA 的表达。结果 Nissl 染色湿示海马区域异位细胞异常聚集。实验组海马区 NKCC 1mRNA 表达明显上调(NKCC1/肌动蛋白的比值,实验组0.70±0.13、对照组0.48±0.09,P<0.01),KCC2 mRNA 表达明显下调(KCC2/肌动蛋白的比值,实验组0.54±0.10、对照组0.81±0.15,P<0.01)。结论 NKCCl mRNA 上调和 KCC2mRNA 下调的共同作用可能与皮质发育障碍致痫密切相关。
OBJECTIVE: To investigate the role of cation-chloride transporter NKCC1 (inbound Na ~ +, K ~ + -2Cl ~ - synergistic transport) and KCC2 (exogenous K ~ + -Cl ~ - synergistic transport) mRNA in epilepsy induced by cortical dysplasia . Methods The model of cortical dysplasia was established by intraperitoneal injection of carmustine (BCNU) on the 17th day of gestation in SD rats. The pathological changes of P60 d pups were observed by Nissl staining. The expression of P60 was detected by reverse transcription polymerase chain reaction (RT-PCR) The expression of NKCC1 and KCC2 mRNA in hippocampus of two groups of male offspring were detected. Results Nissl staining showed abnormal accumulation of ectopic cells in the hippocampus. The expression of NKCC1 mRNA in hippocampus of experimental group was significantly increased (NKCC1 / actin ratio, 0.70 ± 0.13 in experimental group, 0.48 ± 0.09 in control group, P <0.01), and KCC2 mRNA was down-regulated Group 0.54 ± 0.10, control group 0.81 ± 0.15, P <0.01). Conclusions The up-regulation of NKCCl mRNA and the down-regulation of KCC2 mRNA may be closely related to epilepsy induced by cortical dysplasia.