title: Glucocorticoids alter calcium conductances and calcium channel subunit expression in basolateral amygdala neurons.
abstract: 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 alpha1 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.
authors.affiliation: Section Neurobiology, Swammerdam Institute for Life Sciences, University of Amsterdam, the Netherlands Department Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, USA.
authors.forename: Henk
authors.initials: H
authors.lastname: Karst
authors.forename: Suresh
authors.initials: S
authors.lastname: Nair
authors.forename: Els
authors.initials: E
authors.lastname: Velzing
authors.forename: Lisette
authors.initials: L
authors.lastname: Rumpff-van Essen
authors.forename: Eelco
authors.initials: E
authors.lastname: Slagter
authors.forename: Patricia
authors.initials: P
authors.lastname: Shinnick-Gallagher
authors.forename: Marian
authors.initials: M
authors.lastname: Joëls
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000378:metabolism*; D000732:Androstanols / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D020865:Calcium Channels, P-Type / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000494:pharmacology; D005938:Glucocorticoids / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008568:Memory / Q000187:drug effects / Q000502:physiology*; D008569:Memory Disorders / Q000378:metabolism* / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics; D013312:Stress, Physiological / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D000732:Androstanols; D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D020865:Calcium Channels, P-Type; D005938:Glucocorticoids; C432823:NR2C NMDA receptor; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D016194:Receptors, N-Methyl-D-Aspartate; C049154:11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one; D002118:Calcium; D003345:Corticosterone