This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Google Scholar Articles by van Gemert, N. G. Articles by Joëls, M. PubMed PubMed Citation Articles by van Gemert, N. G. Articles by Joëls, M.

Dissociation between Rat Hippocampal CA1 and Dentate Gyrus Cells in Their Response to Corticosterone: Effects on Calcium Channel Protein and Current

Swammerdam Institute for Life Sciences (N.G.G., D.M.M.C., H.K., M.J.), University of Amsterdam, 1098 XH Amsterdam, The Netherlands; Division of Medical Pharmacology (S.v.d.L., O.C.M.), Leiden/Amsterdam Center for Drug Research and Leiden University Medical Center, 2300 RC Leiden, The Netherlands; and Department of Pharmacology (M.Z., J.W.H.), University of Iowa, Iowa City, Iowa 52242; and Department of Neuroscience and Pharmacology (M.J.), University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands

Address all correspondence and requests for reprints to: Marian Joëls, Swammerdam Institute for Life Sciences, Center for NeuroScience, University of Amsterdam, Kruislaan 320, 1098 SM Amsterdam, The Netherlands. E-mail: M.joels{at}uva.nl.

Stress and corticosterone affect, via glucocorticoid receptors, cellular physiology in the rodent brain. A well-documented example concerns corticosteroid effects on high-voltage activated (L type) calcium currents in the hippocampal CA1 area. We tested whether corticosterone also affects calcium currents in another hippocampal area that highly expresses glucocorticoid receptors, i.e. the dentate gyrus (DG). Remarkably, corticosterone (100 nM, given for 20 min, 1–4.5 hr before recording) did not change high-voltage activated calcium currents in the DG, whereas currents in the CA1 area of the same rats were increased. Follow-up studies revealed that no apparent dissociation between the two areas was observed with respect to transcriptional regulation of calcium channel subunits; thus, in both areas corticosterone increased mRNA levels of the calcium channel-β4 but not the () Ca_v1.2 subunit. At the protein level, however, β4 and Ca_v1.2 levels were significantly up-regulated by corticosterone in the CA1 but not the DG area. These data suggest that stress-induced elevations in the level of corticosterone result in a regionally differentiated physiological response that is not simply determined by the glucocorticoid receptor distribution and that the observed regional differentiation may be caused by a gene involved in the translational machinery or in mechanisms regulating mRNA or protein stability.