Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 107, Issue 32, Pages 14449-14454Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0914381107
Keywords
basolateral amygdala; glucocorticoid receptor; glutamate; miniature excitatory postsynaptic current; mineralocorticoid receptor
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Funding
- Dutch Organization for Scientific Research (NWO-ALW) [817.02.017]
- Deutsche Forschungsgemeinschaft [SFB 636]
- European Union [LSHM-CT-2005-018562]
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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.
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