Rapid corticosteroid actions on synaptic plasticity in the mouse basolateral amygdala: Relevance of recent stress history and beta-adrenergic signaling

R. A. Sarabdjitsingh*, M. Joels

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

5 Citations (Scopus)

Abstract

The rodent stress hormone corticosterone rapidly enhances long-term potentiation in the CM hippocampal area, but leads to a suppression when acting in a more delayed fashion. Both actions are thought to contribute to stress effects on emotional memory. Emotional memory formation also involves the basolateral amygdala, an important target area for corticosteroid actions. We here (1) investigated the rapid effects of corticosterone on amygdalar synaptic potentiation, (2) determined to what extent these effects depend on the mouse's recent stress history or (3) on prior beta-adrenoceptor activation; earlier studies at the single cell level showed that especially a recent history of stress changes the responsiveness of basolateral amygdala neurons to corticosterone. We report that, unlike the hippocampus, stress enhances amygdalar synaptic potentiation in a slow manner. In vitro exposure to 100 nM corticosterone quickly decreases synaptic potentiation, and causes only transient potentiation in tissue from stressed mice. This transient type of potentiation is also seen when beta-adrenoceptors are blocked during stress and this is further exacerbated by subsequent in vitro administered corticosterone. We conclude that stress and corticosterone change synaptic potentiation in the basolateral amygdala in a manner opposite to that seen in the hippocampus and that renewed exposure to corticosterone only allows induction of non-persistent forms of synaptic potentiation. (C) 2013 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)168-175
Number of pages8
JournalNeurobiology of Learning and Memory
Volume112
DOIs
Publication statusPublished - Jul-2014
Externally publishedYes

Keywords

  • Stress
  • LTP
  • Basolateral amygdala
  • Corticosterone
  • Propranolol
  • LONG-TERM POTENTIATION
  • DENTATE GYRUS
  • HORMONE CORTICOSTERONE
  • PREFRONTAL CORTEX
  • PREDATOR STRESS
  • FEAR MEMORY
  • RAT-BRAIN
  • RECEPTORS
  • CONSOLIDATION
  • TRANSMISSION

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