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功能性异位神经叶通过PI3K/AKT信号通路增加GAP-43表达,以减轻大鼠垂体柄损伤后的中枢性尿崩症。

Functional ectopic neural lobe increases GAP-43 expression via PI3K/AKT pathways to alleviate central diabetes insipidus after pituitary stalk lesion in rats.

作者信息

Feng Zhanpeng, Ou Yichao, Zhou Mingfeng, Wu Guangsen, Ma Linzi, Zhang Yuan, Liu Yawei, Qi Songtao

机构信息

Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.

First Medical Institute, Southern Medical University, Guangzhou, China.

出版信息

Neurosci Lett. 2018 Apr 23;673:1-6. doi: 10.1016/j.neulet.2018.02.038. Epub 2018 Feb 24.

DOI:10.1016/j.neulet.2018.02.038
PMID:29486290
Abstract

Central diabetes insipidus can occur after hypothalamic-hypophyseal tract injury. This injury is linked with a deficit in circulating vasopressin and oxytocin, which are produced in the supraoptic nuclei and the hypothalamic paraventricular nuclei. Previous studies indicate that an ectopic neural lobe forms after pituitary stalk lesion in rats, and while the relationship between an ectopic neural lobe and CDI outcomes is unclear, the underlying mechanisms are also unknown. Here, we report that two different CDI characteristics are shown in rats that underwent pituitary stalk electric lesion and are defined by two different groups classified as the recovery group and the no-recovery group. Rats showed an enlarged functional ectopic neural lobe at the lesion site with a low CDI index. Moreover, growth associated protein-43, p-PI3K and p-AKT were up-regulated in the unmyelinated fibers of the ectopic neural lobe. Our findings suggest that the enlarged structure formed a functional ectopic neural lobe after the pituitary stalk lesion, and its regeneration might influence the CDI outcome. This regeneration might be due to an increase in GAP-43 expression through the PI3K/AKT pathway.

摘要

中枢性尿崩症可发生在下丘脑 - 垂体束损伤后。这种损伤与循环中抗利尿激素和催产素的缺乏有关,它们由视上核和下丘脑室旁核产生。先前的研究表明,大鼠垂体柄损伤后会形成异位神经叶,虽然异位神经叶与中枢性尿崩症结局之间的关系尚不清楚,但其潜在机制也未知。在此,我们报告,接受垂体柄电损伤的大鼠表现出两种不同的中枢性尿崩症特征,并由分为恢复组和未恢复组的两个不同组别定义。大鼠在损伤部位出现功能性异位神经叶增大,中枢性尿崩症指数较低。此外,生长相关蛋白 - 43、p - PI3K和p - AKT在异位神经叶的无髓纤维中上调。我们的研究结果表明,垂体柄损伤后形成的增大结构构成了功能性异位神经叶,其再生可能影响中枢性尿崩症的结局。这种再生可能是由于通过PI3K/AKT途径使生长相关蛋白 - 43表达增加所致。

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