The interplay between rapid and slow corticosteroid actions in brain

Marian Joels*, Natasha Pasricha, Henk Karst

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

51 Citations (Scopus)

Abstract

Stress causes the release of many transmitters and hormones, including corticosteroids. These molecules enter the brain and exert their effects through the mineralo- and glucocorticoid receptor. The former receptor plays an important role in neuronal stability. However, it also mediates rapid non-genomic corticosteroid effects that in synergy with other stress mediators activate limbic cells and promote behavioral choices allowing the organism to quickly respond to the imminent danger. Glucocorticoid receptors primarily mediate slow genomic effects, for instance in the hippocampus and prefrontal cortex, which are thought to contribute to contextual and higher cognitive aspects of behavioral performance several hours after stress. Rapid and slow effects interact and collectively contribute to successful behavioral adaptation. Long-term disturbances in the release pattern of corticosteroid hormones and in the responsiveness of their receptors give rise to structural and functional changes in neuronal properties which may contribute to the expression of psychopathology. (C) 2013 Elsevier By. All rights reserved.

Original languageEnglish
Pages (from-to)44-52
Number of pages9
JournalEuropean Journal of Pharmacology
Volume719
Issue number1-3
DOIs
Publication statusPublished - 5-Nov-2013
Externally publishedYes

Keywords

  • Corticosterone
  • Hippocampus
  • Amygdala
  • Genemic
  • Non-genomic
  • Adrenalectomy
  • Chronic stress
  • DENTATE GRANULE CELLS
  • STRESS HORMONE CORTICOSTERONE
  • BASOLATERAL AMYGDALA NEURONS
  • LONG-TERM POTENTIATION
  • MINERALOCORTICOID RECEPTORS
  • GLUTAMATERGIC TRANSMISSION
  • SYNAPTIC POTENTIATION
  • PREFRONTAL CORTEX
  • CALCIUM CURRENTS
  • WORKING-MEMORY

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