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在大鼠中,发育过程中的17-OHPC暴露会扰乱由中皮层临性多巴胺系统调节的行为

Paige L Graney¹, Michael Y Chen², Ruth I Wood²

¹Department of Psychology & Center for Neuroscience Research, University at Albany, Albany, NY, USA.

Pharmacology, biochemistry, and behavior

|October 5, 2024

概括

在雄性大鼠中,对17α-hydroxyprogesterone caproate (17-OHPC) 的发育暴露改变了决策和潜伏抑制. 这种合成孕激素可能会影响后代的神经发育,特别是多巴胺D2受体功能.

科学领域:

神经科学是一个神经科学.
发展生物学发展生物学
药理学药理学是指药理学的学科.

背景情况:

17α-hydroxyprogesterone caproate (17-OHPC) 用于减少早产的发生.
17-OHPC穿过胎盘,但其对胎儿神经发育的影响在很大程度上是未知的.
在老鼠中,新生儿暴露会破坏中皮质皮质临性多巴胺路径和相关行为.

研究的目的:

为了研究发育期17-OHPC暴露对由中皮层临性多巴胺基系统调解的认知行为的影响.
为了检查多巴胺D2受体在17-OHPC诱导的行为改变中的作用.

主要方法:

大鼠在发育过程中暴露于17-OHPC.
认知任务包括延迟折扣,有条件的味道厌恶 (CTA) 与潜伏抑制,以及莫里斯水迷宫 (MWM).
在延迟折扣期间,使用Eticlopride和Quinpirole挑战来评估多巴胺D2受体功能.

主要成果:

17-OHPC暴露改变了延迟贴现任务中的决策,并在CTA后降低了潜伏抑制.
在MWM中没有观察到对空间学习和记忆的显著影响.
暴露于17-OHPC的老鼠对Eticlopride诱导的遗漏的敏感性降低,这表明D2受体功能障碍.

结论:

在成年雄性大鼠中,发育过程中的17-OHPC暴露可以改变特定的认知功能,包括决策和潜伏抑制.
这些发现表明17-OHPC对中皮层临性多巴胺系统的潜在神经发育影响.
需要进一步的研究来了解17-OHPC产前暴露的长期后果和临床影响.

关键词:

延迟贴现是一种延迟贴现.多巴胺D2受体的受体.潜伏抑制是一种潜伏抑制.缺失缺失缺失缺失缺失缺失孕激素是一种前性激素.空间记忆是一种空间记忆.

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