Glucocorticoid effects on the brain: from adaptive developmental plasticity to allostatic overload

Helen Eachus, Soojin Ryu

Research output: Contribution to journalReview articlepeer-review

Abstract

Exposure to stress during early life may alter the developmental trajectory of an animal by a mechanism known as adaptive plasticity. For example, to enhance reproductive success in an adverse environment, it is known that animals accelerate their growth during development. However, these short-term fitness benefits are often associated with reduced longevity, a phenomenon known as the growth rate–lifespan trade-off. In humans, early life stress exposure compromises health later in life and increases disease susceptibility. Glucocorticoids (GCs) are major stress hormones implicated in these processes. This Review discusses the evidence for GC-mediated adaptive plasticity in development, leading to allostatic overload in later life. We focus on GC-induced effects on brain structure and function, including neurogenesis; highlight the need for longitudinal studies; and discuss approaches to identify molecular mechanisms mediating GC-induced alteration of the brain developmental trajectory leading to adult dysfunctions. Further understanding of how stress and GC exposure can alter developmental trajectories at the molecular and cellular level is of critical importance to reduce the burden of mental and physical ill health across the life course.
Original languageEnglish
Article numbereb246128
Number of pages11
JournalJournal of Experimental Biology
Volume227
Issue numberSuppl.1
DOIs
Publication statusPublished - 7 Mar 2024

Bibliographical note

Copyright © 2024. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

Keywords

  • Allostasis
  • Stress
  • Neurogenesis
  • Neurodevelopment
  • Cortisol
  • Phenotypic plasticity

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