Mineralocorticoid receptors are indispensable for nongenomic modulation of hippocampal glutamate transmission by corticosterone

Proceedings of the National Academy of Sciences of the United States of America - Tập 102 Số 52 - Trang 19204-19207 - 2005
Henk Karst1, Stefan Berger1, Marc Turiault1, François Tronche1, Günther Schütz1, Marian Joëls1
1Swammerdam Institute for Life Sciences, Center for Neurosciences (SILS–CNS), University of Amsterdam, Kruislaan 320, 1098 SM Amsterdam, The Netherlands; German Cancer Research Institute, 69120 Heidelberg, Germany; and Centre National de la Recherche Scientifique FRE 2401, College de France, 75231 Paris Cedex, France

Tóm tắt

The adrenal hormone corticosterone transcriptionally regulates responsive genes in the rodent hippocampus through nuclear mineralocorticoid and glucocorticoid receptors. Via this genomic pathway the hormone alters properties of hippocampal cells slowly and for a prolonged period. Here we report that corticosterone also rapidly and reversibly changes hippocampal signaling. Stress levels of the hormone enhance the frequency of miniature excitatory postsynaptic potentials in CA1 pyramidal neurons and reduce paired-pulse facilitation, pointing to a hormone-dependent enhancement of glutamate-release probability. The rapid effect by corticosterone is accomplished through a nongenomic pathway involving membrane-located receptors. Unexpectedly, the rapid effect critically depends on the classical mineralocorticoid receptor, as evidenced by the effectiveness of agonists, antagonists, and brain-specific inactivation of the mineralocorticoid but not the glucocorticoid receptor gene. Rapid actions by corticosterone would allow the brain to change its function within minutes after stress-induced elevations of corticosteroid levels, in addition to responding later through gene-mediated signaling pathways.

Từ khóa


Tài liệu tham khảo

Dallman, M. F., Akana, C. S., Cascio, D. N., Darlington, L. & Jacobson, N. (1987) Recent Prog. Horm. Res. 43, 113-173.2819993

10.1038/nrn1683

10.1016/0092-8674(95)90201-5

10.1016/S0303-7207(98)00208-1

10.1038/79910

10.1159/000126440

10.3109/10253899809167281

10.1046/j.1460-9568.1999.00668.x

10.1523/JNEUROSCI.23-12-04850.2003

10.1037/0735-7044.118.5.1062

10.1126/science.2063198

10.1038/12703

10.1152/jn.00143.2005

10.1038/341230a0

10.1038/307462a0

10.1016/0014-2999(88)90131-8

10.1016/S0028-3908(96)00156-6

10.1152/physrev.00003.2003

10.1126/science.173.3992.123

10.1113/jphysiol.1996.sp021204

De Kloet, E. R. (1991) Front. Neuroendocrinol. 12, 95-164.

10.1016/0885-4505(89)90006-6

10.1159/000126135

10.1242/jcs.109.4.787

10.1073/pnas.95.6.2973

10.1210/mend.15.7.0659

10.1677/joe.0.1320305

10.1210/mend.16.1.0748

10.1523/JNEUROSCI.12-08-03217.1992

10.1016/j.brainres.2005.02.068

10.1038/nsmb939

10.1046/j.1460-9568.2000.00878.x

Thông tin
Thông tin xuất bản

Proceedings of the National Academy of Sciences of the United States of America

Tập 102 Số 52

19204-19207

Thông tin tác giả