Department of Translational Neuroscience, Brain Center Rudolf Magnus, UMC Utrecht, Utrecht, 3584 CG, The Netherlands.
Swammerdam Institute for Life Sciences-Center for Neuroscience, University of Amsterdam, Amsterdam, 1090 GE, The Netherlands.
eNeuro. 2017 Nov 2;4(5). doi: 10.1523/ENEURO.0253-17.2017. eCollection 2017 Sep-Oct.
Early life adversity is a well-known risk factor for behavioral dysfunction later in life, including the formation of contextual memory; it is also (transiently) accompanied by hyperactivity of the stress system. We tested whether mifepristone (MIF) treatment, which among other things blocks glucocorticoid receptors (GRs), during the prepubertal period [postnatal days (PND)26-PND28] normalizes memory deficits in adult male rats exposed to 24-h maternal deprivation (MD) at PND3. MD reduced body weight gain and increased basal corticosterone (CORT) levels during the PND26, but not in adulthood. In adulthood, contextual memory formation of MD compared to noMD (i.e., control) male rats was significantly impaired. This impairment was fully prevented by MIF treatment at PND26-PND28, whereas MIF by itself did not affect behavior. A second behavioral test, a rodent version of the Iowa Gambling Task (rIGT), revealed that flexible spatial learning rather than reward-based aspects of performance was impaired by MD; the deficit was prevented by MIF. Neuronal activity as tested by c-Fos staining in the latter task revealed changes in the right hippocampal-dorsomedial striatal pathway, but not in prefrontal areas involved in reward learning. Follow-up electrophysiological recordings measuring spontaneous glutamate transmission showed reduced frequency of miniature postsynaptic excitatory currents in adult CA1 dorsal hippocampal and enhanced frequency in dorsomedial striatal neurons from MD versus noMD rats, which was not seen in MIF-treated rats. We conclude that transient prepubertal MIF treatment normalizes hippocampus-striatal-dependent contextual memory/spatial learning deficits in male rats exposed to early life adversity, possibly by normalizing glutamatergic transmission.
早期生活逆境是行为功能障碍的一个已知风险因素,包括情景记忆的形成;它也(暂时地)伴随着应激系统的过度活跃。我们测试了米非司酮(MIF)治疗是否能在青春期前[产后第 26 天(PND26)至第 28 天(PND28)]恢复经历过 24 小时母鼠剥夺(MD)的成年雄性大鼠的记忆缺陷,该治疗除其他作用外还阻断糖皮质激素受体(GRs)。MD 减少了体重增加,并在 PND26 时增加了基础皮质酮(CORT)水平,但在成年时没有增加。在成年期,与未 MD(即对照)雄性大鼠相比,MD 雄性大鼠的情景记忆形成明显受损。这种损伤完全被 PND26-PND28 时的 MIF 治疗所预防,而 MIF 本身不会影响行为。第二项行为测试,一种啮齿动物版的爱荷华赌博任务(rIGT),表明灵活的空间学习而不是基于奖励的表现受损是由 MD 引起的;MIF 预防了这种缺陷。在后者的任务中,通过 c-Fos 染色测试神经元活动表明,右侧海马背侧纹状体通路发生了变化,但参与奖励学习的前额叶区域没有变化。后续的测量自发谷氨酸传递的电生理记录显示,成年 CA1 背侧海马中的小突触后兴奋性电流的频率降低,而 MD 大鼠的背侧纹状体神经元的频率增加,而在 MIF 处理的大鼠中则没有看到这种情况。我们得出的结论是,青春期前短暂的 MIF 治疗可以使经历过早期生活逆境的雄性大鼠的海马-纹状体依赖的情景记忆/空间学习缺陷正常化,这可能是通过正常化谷氨酸传递来实现的。