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红藻氨酸诱导癫痫发作后大鼠下丘脑精氨酸加压素合成的上调。

Upregulation of arginine vasopressin synthesis in the rat hypothalamus after kainic acid-induced seizures.

机构信息

Department of Rehabilitation Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.

出版信息

Brain Res. 2011 Nov 18;1424:1-8. doi: 10.1016/j.brainres.2011.09.030. Epub 2011 Sep 22.

Abstract

We examined the effects of kainic acid (KA)-induced seizures on arginine vasopressin (AVP) gene expression in the paraventricular (PVN) and the supraoptic nuclei (SON) of normal rats using in situ hybridization histochemistry. We also investigated the expression of the AVP-enhanced green fluorescent protein (eGFP) fusion gene after KA-induced seizures in transgenic rats. AVP heteronuclear (hn) RNA levels in the PVN and the SON were significantly increased at 3h and 24h after subcutaneous (s.c.) administration of KA in normal rats. AVP mRNA levels in the PVN and the SON did not change significantly at 3h, 24h and 1 week after s.c. administration of KA in normal rats. In KA-administered transgenic rats, AVP-eGFP fluorescence in the magnocellular and parvocellular divisions of the PVN and the SON were significantly stronger compared to vehicle-administered transgenic rats. By pretreatment with MK-801 (nonselective N-methyl-D-aspartate, NMDA, receptor antagonist), AVP-eGFP transgenic rats after administration of KA did not show preconvulsive symptoms or convulsions and AVP-eGFP fluorescence in the magnocellular and parvocellular divisions of the PVN and the SON of these rats was significantly reduced. These results suggested that KA-induced increases in AVP transcripts and AVP were prevented by MK801 because seizure activity was prevented or reduced.

摘要

我们使用原位杂交组织化学方法研究了海人酸(KA)诱导的癫痫发作对正常大鼠室旁核(PVN)和视上核(SON)中精氨酸加压素(AVP)基因表达的影响。我们还研究了 KA 诱导的癫痫发作后转基因大鼠中 AVP 增强型绿色荧光蛋白(eGFP)融合基因的表达。在正常大鼠皮下(s.c.)给予 KA 后 3h 和 24h,PVN 和 SON 中的 AVP 异核(hn)RNA 水平显著增加。在正常大鼠皮下给予 KA 后 3h、24h 和 1 周,PVN 和 SON 中的 AVP mRNA 水平没有明显变化。在 KA 给药的转基因大鼠中,与给予载体的转基因大鼠相比,PVN 和 SON 的大细胞和小细胞部分中的 AVP-eGFP 荧光明显增强。通过 MK-801(非选择性 N-甲基-D-天冬氨酸,NMDA 受体拮抗剂)预处理,给予 KA 后的 AVP-eGFP 转基因大鼠没有出现前惊厥症状或惊厥,并且这些大鼠的 PVN 和 SON 大细胞和小细胞部分中的 AVP-eGFP 荧光明显减少。这些结果表明,由于癫痫发作活动被预防或减少,MK801 可预防或减少 KA 诱导的 AVP 转录物和 AVP 的增加。

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