Conrad Cheryl D
Deparment of Psychology, Arizona State University, Box 1104, Tempe, 85287-1104, USA.
Behav Cogn Neurosci Rev. 2006 Mar;5(1):41-60. doi: 10.1177/1534582306289043.
Chronic stress produces consistent and reversible changes within the dendritic arbors of CA3 hippocampal neurons, characterized by decreased dendritic length and reduced branch number. This chronic stress-induced dendritic retraction has traditionally corresponded to hippocampus-dependent spatial memory deficits. However, anomalous findings have raised doubts as to whether a CA3 dendritic retraction is sufficient to compromise hippocampal function. The purpose of this review is to outline the mechanism underlying chronic stress-induced CA3 dendritic retraction and to explain why CA3 dendritic retraction has been thought to mediate spatial memory. The anomalous findings provide support for a modified hypothesis, in which chronic stress is proposed to induce CA3 dendritic retraction, which then disrupts hypothalamic-pituitary-adrenal axis activity, leading to dysregulated glucocorticoid release. The combination of hippocampal CA3 dendritic retraction and elevated glucocorticoid release contributes to impaired spatial memory. These findings are presented in the context of clinical conditions associated with elevated glucocorticoids.
慢性应激会在海马体CA3区神经元的树突分支内产生持续且可逆的变化，其特征为树突长度缩短和分支数量减少。传统上，这种慢性应激诱导的树突回缩与依赖海马体的空间记忆缺陷相对应。然而，一些异常发现引发了人们对于CA3区树突回缩是否足以损害海马体功能的质疑。本综述的目的是概述慢性应激诱导CA3区树突回缩的潜在机制，并解释为何一直认为CA3区树突回缩介导空间记忆。这些异常发现为一个修正后的假说提供了支持，该假说认为慢性应激会诱导CA3区树突回缩，进而扰乱下丘脑-垂体-肾上腺轴的活动，导致糖皮质激素释放失调。海马体CA3区树突回缩与糖皮质激素释放增加共同导致空间记忆受损。这些发现是在与糖皮质激素升高相关的临床病症背景下呈现的。
