Abstract
Prolonged exposure to glucocorticoid stress hormones, such as cortisol in humans, has been associated with structural and functional changes in the hippocampus. The majority of research demonstrating these associations in humans has been conducted in adult, clinical, or severely maltreated populations, with little research investigating these effects in young or more typically developing populations. The present study sought to address this gap by investigating longitudinal associations between preschool (3−5 years) and concurrent (5–9 years) cortisol reactivity to a laboratory stressor and hippocampal functional connectivity during a passive viewing fMRI scan. Results showed that, after controlling for concurrent cortisol reactivity, greater total cortisol release in response to a stressor during preschool predicted increased anterior and posterior hippocampal connectivity with the precuneus and cingulate gyrus at school-age. These findings are consistent with literature from adult and non-human investigations and suggest lasting impacts of early stress physiology on the brain.
Highlights
Glucocorticoid stress hormones, such as cortisol, are released as part of a normal physiological response to stress through the functions of the hypothalamic-pituitary-adrenal (HPA) axis
These stress hormones are beneficial to humans when released at optimal times and allowed to fluctuate normally as they enable adaptive coping to stressors (Smith and Vale, 2006)
Impacts of excessive cortisol are evident in regions with high densities of glucocorticoid receptors, such as the hippocampus (Virgin et al, 1991), a structure implicated in an array of processes, including episodic memory, stress regulation, and spatial navigation (Chersi and Burgess, 2015; Herman et al, 2016; Tulving and Markowitsch, 1998)
Summary
Glucocorticoid stress hormones, such as cortisol, are released as part of a normal physiological response to stress through the functions of the hypothalamic-pituitary-adrenal (HPA) axis. These stress hormones are beneficial to humans when released at optimal times and allowed to fluctuate normally as they enable adaptive coping to stressors (Smith and Vale, 2006). Impacts of excessive cortisol are evident in regions with high densities of glucocorticoid receptors, such as the hippocampus (Virgin et al, 1991), a structure implicated in an array of processes, including episodic memory, stress regulation, and spatial navigation (Chersi and Burgess, 2015; Herman et al, 2016; Tulving and Markowitsch, 1998). Excessive levels of cortisol can suppress neurogenesis, inhibit synaptogenesis, and result in atypical dendritic branching and axon development (Gould and Tanapat, 1999; Woolley et al, 1990)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
