| 贺嘉 朱雨岚 孙威 郑姣琳 勾海燕 陈岩.拉莫三嗪对GHB 致失神发作大鼠脑内HCN1、HCN2表达的影响[J].,2016,16(3):423-426 |
| 拉莫三嗪对GHB 致失神发作大鼠脑内HCN1、HCN2表达的影响 |
| The Influence of Lamotrigine on Protein HCN1 and HCN2 Expression inBrain of GHB Induced Rat Absence Model |
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| DOI： |
| 中文关键词: 拉莫三嗪 失神发作 HCN1 HCN2 皮层脑电图 |
| 英文关键词: Lamotrigine Absence seizure HCN1 HCN2 ECoG |
| 基金项目:黑龙江省留学归国基金项目（LC2011C19）；黑龙江省卫生厅科研课题（2007-330） |
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| 中文摘要: |
| 目的：观察拉莫三嗪对r- 羟丁酸（GHB）致失神发作大鼠脑电及脑内超极化激活环核苷酸门控阳离子通道(HCN)的亚型
HCN1、HCN2 表达变化的影响，探讨拉莫三嗪抗失神癫痫的可能作用机制。方法：健康成年雄性SD 大鼠，随机分为空白对照组，
模型组，拉莫三嗪治疗组（低剂量组为8 mg/(kg·d)、中剂量组为12 mg/(kg·d)、高剂量组为24 mg/(kg·d))，每组7 只。空白对照组及
模型组每日应用0.25 %的甲基纤维素钠溶液灌胃，治疗组每日应用0.25 %的甲基纤维素钠溶液配制的浓度为2 mg/mL的拉莫三
嗪混悬液灌胃。手术埋置皮层脑电电极。腹腔注射GHB的前体r- 丁内酯(GBL) 200 mg/kg制作大鼠失神发作模型，并监测脑电。
免疫组化法检测皮层HCN1及丘脑HCN2 的表达。结果：皮层脑电图拉莫三嗪治疗组比模型组失神发作的潜伏期延长，最高波幅
降低（P<0.05）。模型组皮质HCN1 比空白对照组表达减少，而拉莫三嗪高、中剂量组皮质HCN1 比模型组表达增加（P<0.05）。模型
组丘脑HCN2 表达减少，与空白对照组及治疗组相比，差异有统计学意义。结论：拉莫三嗪可以改善GHB 致失神发作模型脑电图
的异常表现；拉莫三嗪抗失神癫痫作用可能与调节HCN表达有关。 |
| 英文摘要: |
| Objective:To investigate the influence of lamotrigine on protein HCN1 and HCN2 expression in brain of Gamma-Hydroxybutyrate
(GHB) induced rat absence model, and to explore the antiepileptic mechanismof lamotrigine to absence seizure.Methods:Healthy adult Sprague-Dawley rats were randomly divided into 5 groups: normal group, model group, lamotrigine pretreatment group
(low dose group8 mg/(kg·d), medium dose group 12 mg/(kg·d) and high dose group 24 mg/(kg·d)), 7 rats in each group. The rats in the
normal and model groups were gavaged with sodium methylcellulose once a day. Simultaneously, the rats in the pretreatment groups
were gavaged with the corresponding dosage of lamotrigine. Electrode screws were surgically implanted on the dural surfaces for electrocorticogrammonitoring.
The rat absence models were established by injecting intraperitoneally with the GBL (200 mg/kg), and the electrocorticogram(
ECoG) abnormalities were monitored. The expressions of HCN1 and HCN2 in cortex and thalamus were detected by immunohistochemical
assay.Results:The pretreatment group had a longer lantency and lower maximum wave amplitude compared with
the model group (P<0.05). Compared with the normal group, the HCN1 expression in cortex of the model group decreased. The expression
of cortical HCN1 in groups with medium and high dose lamotrigine increased than the model group (P<0.05). The expression of
HCN2 in thalamus in the model group decreased. The differences had statistical significance compared with the normal and pretreatment
groups.Conclusion:Lamotrigine has the efficacy in improving the ECoG finding of the GHB induced rat absence model; The
antiepileptic mechanismof lamotrigine to absence seizure may be related to HCN. |
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