Barfield Elizabeth T, Sequeira Michelle K, Parsons Ryan G, Gourley Shannon L
Departments of Pediatrics and Psychiatry, Emory University School of Medicine, Yerkes National Primate Research Center, Emory University, Atlanta, GA, United States.
Graduate Training Programs in Neuroscience, Emory University, Atlanta, GA, United States.
Front Neuroanat. 2020 Sep 8;14:45. doi: 10.3389/fnana.2020.00045. eCollection 2020.
Considerable evidence indicates that chronic stress and excess glucocorticoids induce neuronal remodeling in prefrontal cortical (PFC) regions. Adolescence is also characterized by a structural reorganization of PFC neurons, yet interactions between stress- and age-related structural plasticity are still being determined. We quantified dendritic spine densities on apical dendrites of excitatory neurons in the medial prefrontal cortex, prelimbic subregion (PL). Densities decreased across adolescent development, as expected, and spine volume increased. Unexpectedly, exposure to excess corticosterone (CORT) throughout adolescence did not cause additional dendritic spine loss detectable in adulthood. As a positive control dendrite population expected to be sensitive to CORT, we imaged neurons in the orbitofrontal cortex (OFC), confirming CORT-induced dendritic spine attrition on basal arbors of layer V neurons. We next assessed the effects of acute, mild stress in adulthood: On PL neurons, an acute stressor increased the density of mature, mushroom-shaped spines. Meanwhile, on OFC neurons, dendritic spine volumes and lengths were lower in mice exposed to both CORT and an acute stressor (also referred to as a "double hit"). In sum, prolonged exposure to excess glucocorticoids during adolescence can have morphological and also metaplastic consequences, but they are not global. Anatomical considerations are discussed.
大量证据表明,慢性应激和过量的糖皮质激素会诱导前额叶皮质(PFC)区域的神经元重塑。青春期的特征还包括PFC神经元的结构重组,然而,应激和年龄相关的结构可塑性之间的相互作用仍有待确定。我们对内侧前额叶皮质前边缘亚区(PL)兴奋性神经元顶树突上的树突棘密度进行了量化。正如预期的那样,在整个青春期发育过程中,树突棘密度下降,而树突棘体积增加。出乎意料的是,在整个青春期暴露于过量的皮质酮(CORT)并不会导致成年期可检测到的额外树突棘丢失。作为预期对CORT敏感的阳性对照树突群体,我们对眶额皮质(OFC)中的神经元进行了成像,证实了CORT诱导的V层神经元基底树突上的树突棘磨损。接下来,我们评估了成年期急性轻度应激的影响:对于PL神经元,急性应激源增加了成熟的蘑菇状树突棘的密度。同时,对于OFC神经元,在同时暴露于CORT和急性应激源(也称为“双重打击”)的小鼠中,树突棘的体积和长度较小。总之,青春期长期暴露于过量的糖皮质激素会产生形态学和化生后果,但并非全局性的。文中讨论了解剖学方面的考虑因素。