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Glucocorticoids alter calcium conductances and calcium channel subunit expression in basolateral amygdala neurons
Author(s) -
Karst Henk,
Nair Suresh,
Velzing Els,
Rumpffvan Essen Lisette,
Slagter Eelco,
ShinnickGallagher Patricia,
Joëls Marian
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02172.x
Subject(s) - basolateral amygdala , amygdala , chemistry , r type calcium channel , neuroscience , calcium channel , t type calcium channel , hippocampus , glucocorticoid receptor , calcium , calcium in biology , voltage dependent calcium channel , p type calcium channel , n type calcium channel , endocrinology , medicine , receptor , biology , glucocorticoid , biochemistry , organic chemistry
Glucocorticoid hormones, which are released in high amounts after stress, enter the brain where they bind to intracellular receptors that are abundant in limbic areas, in particular the hippocampus and amygdala nuclei. Behavioural studies indicate that glucocorticoids modulate learning and memory processes via receptors in the hippocampus and amygdala. So far, the effects of glucocorticoids on amygdala neurons have not been investigated at the cellular and molecular level. We report here that in vitro application of glucocorticoids for 20 min increases 1–4 h later the amplitude of sustained, high‐voltage‐activated calcium currents in principal neurons of the basolateral amygdala. In contrast, the transient, low‐voltage‐activated currents were decreased. We examined whether these functional changes in calcium conductance were accompanied by transcriptional regulation of calcium channel subunits. Analysis of the RNA – collected after recording and then linearly amplified – revealed that glucocorticoid‐mediated increases in sustained calcium currents are associated with a parallel shift in the relative expression of the α 1 subunit constituting the pore of the sustained, high‐voltage‐activated (L‐type) calcium channel. These data indicate that glucocorticoids, probably by selectively targeting genes encoding calcium channel subunits, largely alter the calcium influx into basolateral amygdala neurons. These actions could modify amygdala network function and thus contribute to the behavioural effects exerted by the stress hormones via the basolateral amygdala.