Metaplasticity of amygdalar responses to the stress hormone corticosterone.
High levels of corticosteroids (as circulate after stress) quickly and reversibly enhance hippocampal glutamatergic transmission via nongenomic 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.
Karst
Henk
H
Department of Neuroscience and Pharmacology, University Medical Center Utrecht, 3508 AB, Utrecht, The Netherlands. h.karst@umcutrecht.nl
Berger
Stefan
S
Erdmann
Gitta
G
Schütz
Günther
G
Joëls
Marian
M
D000679:Amygdala / Q000166:cytology / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology*; D019706:Excitatory Postsynaptic Potentials; D018698:Glutamic Acid; D053444:Inhibitory Postsynaptic Potentials; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D018161:Receptors, Mineralocorticoid / Q000378:metabolism; D013312:Stress, Physiological / Q000502:physiology; D055366:Synaptic Potentials / Q000502:physiology*; D009435:Synaptic Transmission
D018161:Receptors, Mineralocorticoid; D018698:Glutamic Acid; D003345:Corticosterone