Abstract
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.
Highlights
IntroductionGlucocorticoids (primarily corticosterone in rodents) are principal mediators of the stress response
Glucocorticoids are principal mediators of the stress response
We focused on basal arbors because dendritic spines on these arbors are sensitive exogenous CORT exposure in adolescence (Barfield and Gourley, 2019), as well as other adolescent experiences, including olanzapine treatment (Milstein et al, 2013), environmental enrichment (Mychasiuk et al, 2014), and cocaine exposure (DePoy et al, 2017)
Summary
Glucocorticoids (primarily corticosterone in rodents) are principal mediators of the stress response. They mobilize energy stores to enable organisms to cope with stress, and are potent modulators of synaptic plasticity, with precise neurobehavioral effects varying depending on the intensity, duration, context, and developmental timing of stressor exposure. Neuronal Responses to Excess Corticosterone mild, acute stress causes synaptic plasticity in the prefrontal cortex (PFC) and improves certain cognitive functions (Joëls et al, 2006; Popoli et al, 2011; McEwen and Morrison, 2013)—effects generally considered adaptive. Chronic stress or prolonged exposure to elevated glucocorticoids extensively reorganizes PFC neuronal architecture (Leuner and Shors, 2013; McEwen and Morrison, 2013). Chronic stress can impact synaptic plasticity in response to subsequent experiences, an example of stress-induced metaplasticity (Luczynski et al, 2015; Nasca et al, 2015)
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