Metaplasticity of amygdalar responses to the stress hormone corticosterone

Henk Karst*, Stefan Berger, Gitta Erdmann, Guenther Schuetz, Marian Joels

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

258 Citations (Scopus)

Abstract

High levels of corticosteroids (as circulate after stress) quickly and reversibly enhance hippocampal glutamatergic transmission via non-genomic actions requiring mineralocorticoid receptors. Subsequently, the hormone slowly and long-lastingly normalizes hippocampal cell function, through nuclear glucocorticoid receptors. Here we describe a rapid mineralocorticoid receptor-dependent enhancement of glutamatergic transmission in basolateral amygdala neurons. Contrary to the hippocampus, this rapid enhancement is long-lasting, potentially allowing an extended window for encoding of emotional aspects during stressful events. Importantly, the long-lasting change in state of amygdala neurons greatly affects the responsiveness to subsequent surges of corticosterone, revealing a quick suppression of glutamatergic transmission, which requires the glucocorticoid receptor. Responses of basolateral amygdala neurons to the stress hormone corticosterone can thus switch from excitatory to inhibitory, depending on the recent stress history of the organism.

Original languageEnglish
Pages (from-to)14449-14454
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume107
Issue number32
DOIs
Publication statusPublished - 10-Aug-2010
Externally publishedYes

Keywords

  • basolateral amygdala
  • glucocorticoid receptor
  • glutamate
  • miniature excitatory postsynaptic current
  • mineralocorticoid receptor
  • BASOLATERAL AMYGDALA
  • MINERALOCORTICOID RECEPTORS
  • MEMORY
  • CONSOLIDATION
  • PLASTICITY
  • MODULATION
  • ENHANCE
  • BRAIN

Cite this