Department of Psychology, Arizona State University, Box 1104, Tempe, AZ 85287-1104, United States.
Department of Psychology, Arizona State University, Box 1104, Tempe, AZ 85287-1104, United States.
Front Neuroendocrinol. 2018 Apr;49:114-123. doi: 10.1016/j.yfrne.2018.02.005. Epub 2018 Feb 8.
Chronic stress results in functional and structural changes to the brain and especially the hippocampus. Decades of research have provided insights into the mechanisms by which chronic stress impairs hippocampal-mediated cognition and the corresponding reduction of hippocampal CA3 apical dendritic complexity. Yet, when chronic stress ends and time passes, which we refer to as a "post-stress rest period," hippocampal-mediated spatial memory deficits begin to improve and CA3 apical dendritic arbors increase in complexity. The processes by which the hippocampus improves from a chronically stressed state are not simply the reversal of the mechanisms that produced spatial memory deficits and CA3 apical dendritic retraction. This review will discuss our current understanding of how a chronically stressed hippocampus improves after a post-stress rest period. Untangling the mechanisms that allow for this post-stress plasticity is a critical next step in understanding how to promote resilience in the face of stressors.
慢性应激会导致大脑（尤其是海马体）的功能和结构发生变化。几十年来的研究为我们提供了深入了解慢性应激损害海马介导的认知和相应的海马 CA3 树突棘复杂性减少的机制。然而，当慢性应激结束并随着时间的推移，即我们所称的“应激后休息期”，海马介导的空间记忆缺陷开始改善，CA3 树突棘复杂性增加。海马体从慢性应激状态中恢复的过程并不仅仅是产生空间记忆缺陷和 CA3 树突棘回缩的机制的逆转。这篇综述将讨论我们目前对慢性应激后应激休息期海马体如何改善的理解。理清允许这种应激后可塑性的机制是理解如何在面对应激源时促进韧性的关键下一步。
