Nacher J, Pham K, Gil-Fernandez V, McEwen B S
Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021, USA.
Neuroscience. 2004;126(2):503-9. doi: 10.1016/j.neuroscience.2004.03.038.
Stress and stress-related hormones induce structural changes in neurons of the adult CNS. Neurons in the hippocampus, the amygdala and the prefrontal cortex undergo neurite remodeling after chronic stress. In the hippocampus some of these effects can be mimicked with chronic administration of adrenal steroids. These changes in neuronal structure may be mediated by certain molecules related to plastic events such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). The expression of PSA-NCAM persists in the adult hippocampus and it is up-regulated after chronic stress. The piriform cortex also displays considerable levels of PSA-NCAM during adulthood and indirect evidence suggests that it may also be the target of stress and stress related-hormones. Using immunohistochemistry we have studied the expression of PSA-NCAM and doublecortin (DCX; another protein implicated in neuronal structural plasticity) in the piriform cortex of adult rats subjected either to 21 days of chronic restraint stress or to oral corticosterone administration during the same period. Our results indicate that chronic stress and chronic corticosterone administration have differential effects on the expression of PSA-NCAM and DCX. While chronic stress increases the number of PSA-NCAM- and DCX-immunoreactive cells in the piriform cortex layer II, chronic corticosterone administration decreases these numbers. These findings indicate that stress and adrenal steroids affect the piriform cortex and suggest that in this region, as in the hippocampus, they may induce structural changes. This is a potential mechanism by which stress and corticosterone modulate functions of this limbic region, such as its participation in olfactory memory.
应激及与应激相关的激素会诱导成年中枢神经系统神经元发生结构变化。海马体、杏仁核和前额叶皮质中的神经元在慢性应激后会经历神经突重塑。在海马体中,这些效应中的一些可以通过长期给予肾上腺皮质类固醇来模拟。神经元结构的这些变化可能由某些与可塑性事件相关的分子介导,比如神经细胞黏附分子的多唾液酸化形式(PSA-NCAM)。PSA-NCAM的表达在成年海马体中持续存在,并且在慢性应激后会上调。梨状皮质在成年期也显示出相当水平的PSA-NCAM,间接证据表明它也可能是应激及与应激相关激素的作用靶点。我们运用免疫组织化学方法,研究了成年大鼠梨状皮质中PSA-NCAM和双皮质素(DCX;另一种与神经元结构可塑性有关的蛋白质)的表达,这些成年大鼠分别经历了21天的慢性束缚应激,或在同一时期口服皮质酮。我们的结果表明,慢性应激和长期给予皮质酮对PSA-NCAM和DCX的表达有不同影响。慢性应激会增加梨状皮质第二层中PSA-NCAM和DCX免疫反应阳性细胞的数量,而长期给予皮质酮则会减少这些细胞数量。这些发现表明应激和肾上腺皮质类固醇会影响梨状皮质,并提示在该区域,与在海马体中一样,它们可能会诱导结构变化。这是应激和皮质酮调节这个边缘区域功能(比如其参与嗅觉记忆)的一种潜在机制。