大脑产生的雌激素调节神经发生,学习和记忆与老龄化在雌性大鼠
Yuanyuan Huang1,2, Wuxiang Sun1,2, Fujia Gao1
1Neurobiology Institute, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
Biology
|June 28, 2023
概括
由大脑衍生的17β-雌激醇 (BDE2) 对于维持海马神经发生和老化雌性大鼠的认知功能至关重要. 丧失BDE2会损害神经干细胞活动和学习,特别是在年轻动物中.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 衰老研究研究 衰老研究
背景情况:
- 17β-雌二醇 (E2) 在大脑中合成,但大脑衍生的E2 (BDE2) 在衰老神经生成中的作用尚不清楚.
- 衰老影响海马神经干细胞,神经生成和神经生成,影响认知功能.
研究的目的:
- 在雌性大鼠中调查BDE2对海马神经发生和在老化过程中的质发生的影响.
- 为了确定受损BDE2合成对认知功能的影响.
主要方法:
- 在年龄为1-18个月的雌性大鼠中检查了海马神经干细胞,神经发生和质发生.
- 使用雌性前脑神经芳酶淘汰 (FBN-ARO-KO) 鼠和莱特治疗来抑制E2合成.
- 评估了CREB-BDNF激活和神经纤维,脊髓蛋白和PSD95.5的蛋白质水平.
- 评估海马体依赖的空间学习和记忆.
主要成果:
- 神经干细胞数量随着年龄的增长而下降 (14个月),而天体细胞和微质细胞活化增加.
- 神经发生率从1个月大开始急剧下降.
- FBN-ARO-KO抑制了牙状神经发生,并且在1个月后与莱特一起降低了神经发生.
- BDE2缺乏抑制了CREB-BDNF激活,并降低了关键突触蛋白水平.
- 在青少年和成年KO大鼠中,空间学习和记忆受损.
结论:
- 在女性衰老过程中,BDE2在支持海马神经发生和质发生方面发挥着至关重要的作用.
- BDE2对于维持学习和记忆功能至关重要,特别是在年轻和中年雌性大鼠中.
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