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J Biol Chem, Vol. 275, Issue 2, 1321-1326, January 14, 2000

Regulation of the Rat Serotonin-1A Receptor Gene by Corticosteroids^*

Sacha Wissink, Onno Meijer^§, David Pearce^¶, Bart van der Burg, and Paul T. van der Saag

From the  Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Uppsalalaan 8, 3584 CT Utrecht, the Netherlands, the ^§ Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, University of Leiden, 2300 RA Leiden, the Netherlands, and the ^¶ Department of Medicine, Division of Nephrology, University of California, San Francisco, California 94143

Dysregulation of the serotonergic system and abnormalities of the hypothalamic-pituitary-adrenal axis function have been implicated to be involved in neuropsychiatric disorders. Serotonin-1A receptors have been shown to be suppressed by corticosteroid hormones in a variety of animal studies. This effect may play a central role in the pathophysiology of depression. However, little is known about the molecular mechanism underlying this suppressive effect of corticosteroids. Here, we show by functional analysis of the promoter region of the rat serotonin-1A receptor gene that two NF-B elements in the promoter contribute to induced transcription of the rat serotonin-1A receptor gene. Furthermore, we show that corticosteroids repress this NF-B-mediated induction of transcription. Remarkably, we observed that only the glucocorticoid receptor and not the mineralocorticoid receptor was able to mediate this repressive effect of corticosteroids. We argue that negative cross-talk between the glucocorticoid receptor and NF-B may provide a basis for the molecular mechanism underlying the negative action of corticosteroids on serotonin signaling in the brain.

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