Dexamethasone rapidly induces Kv1.5 K + channel gene transcription and expression in clonal pituitary cells

• Published in: Neuron (Cambridge, Mass.) Vol. 11; no. 2; pp. 359 - 369
• Main Authors: Takimoto, Koichi, Fomina, Alla F., Gealy, Robert, Trimmer, James S., Levitan, Edwin S.
• Format: Journal Article
• Language: English
• Published: Cambridge, MA Elsevier Inc 01.08.1993; Cell Press
• Subjects: Animals; Biological and medical sciences; Clone Cells; Dexamethasone - pharmacology; Fundamental and applied biological sciences. Psychology; Hormones and neuropeptides. Regulation; Hypothalamus. Hypophysis. Epiphysis. Urophysis; Pituitary Gland - cytology; Pituitary Gland - metabolism; Potassium Channels - genetics; Potassium Channels - metabolism; RNA, Messenger - metabolism; Transcription, Genetic - drug effects; Vertebrates: endocrinology; Vertebrata; Endocrine gland; Mammalia; Dexamethasone; Rat; Transcription; Rodentia; Pituitary gland; Ionic channel; Gene expression; Glucocorticoid; Potassium
• ISSN: 0896-6273; 1097-4199
• DOI: 10.1016/0896-6273(93)90191-S

Glucocorticoids specifically increase Kv1.5 K + channel mRNA in normal and clonal (GH 3) rat pituitary cells. Here, we demonstrate that dexamethasone, a glucocorticoid agonist, rapidly induces Kv1.5 gene transcription, but does not affect Kv1.5 mRNA turnover t 1 2 ≈ 0.5 hr ) in GH 3 cells. Immunoblots indicate that the steroid also increases the expression of the 76 kd Kv1.5 protein 3-fold within 12 hr without altering its half-life ( t 1 2 ≈ 4 hr ). In contrast, Kv1.4 protein expression is unaffected. Finally, we find that the induction of Kv1.5 protein is associated with an increase in a noninactivating component of the voltage-gated K + current. Our results indicate that hormones and neurotransmitters may act within hours to regulate excitability by controlling K + channel gene expression.