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在小鼠中轻度妊娠性甲状腺功能下降症对神经内分泌系统具有暂时的发育效应和长期后果

Clarisse Quignon¹, Annika Backer¹, Jessica Kearney¹

¹National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.

Thyroid : official journal of the American Thyroid Association

|December 27, 2024

概括

怀孕期间母亲的轻度甲状腺激素缺乏症暂时减少胎儿的GnRH神经元发育. 成年后代表现出持久的神经内分泌变化,影响生殖健康.

科学领域:

神经内分泌学神经内分泌学
发育生物学发展生物学
生殖科学生殖科学

背景情况:

甲状腺激素 (TH) 对胎儿大脑发育至关重要,严重的功能障碍会导致疾病.
环境TH干扰者需要了解轻度妊娠TH不足的影响.
早期发育,包括生殖网络,依赖于孕期中期之前的孕妇TH.

研究的目的:

为了研究母亲轻度甲状腺功能低下症对性腺激素释放激素 (GnRH) 神经元发育的影响.
评估长期的神经内分泌功能影响暴露于妊娠性甲状腺功能低下症的后代.
用小鼠模型研究怀孕期间的亚临床甲状腺功能障碍.

主要方法:

在小鼠模型中使用甲基马 (MMI) 诱导妊娠期甲状腺功能低下症.
对E12/13胚胎中GnRH神经元数量,迁移和增殖的分析.
评估后代的断奶后生长,雌性周期和成人神经内分泌标志物.

主要成果:

MMI治疗减少了幼大小和胚胎GnRH神经元数量,特别是在鼻器官 (VNO).
在VNO中细胞增殖减少与较少的GnRH神经元相关;在体外,T3缺失减弱了细胞增殖.
成人后代表现出正常的生长和循环,但在弧形核中增加了雌激素受体α表达,在成年时具有补偿性的GnRH神经元数量.

结论:

轻微的妊娠TH中断暂时影响VNO中的GnRH神经元增殖.
长期的神经内分泌系统的影响在母亲轻度甲状腺功能低下症的后代中观察到.
补偿机制在成年时恢复了GnRH神经元数量,但微妙的神经内分泌变化仍然存在.

关键词:

在GnRH神经元中.胚胎发育过程中的胚胎.孕产妇的甲状腺功能低下症神经内分泌学神经内分泌学生殖生殖的繁殖.甲状腺激素甲状腺激素

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