Takimoto K, Fomina A F, Gealy R, Trimmer J S, Levitan E S
Department of Pharmacology, University of Pittsburgh, Pennsylvania 15261.
Neuron. 1993 Aug;11(2):359-69. doi: 10.1016/0896-6273(93)90191-s.
Glucocorticoids specifically increase Kv1.5 K+ channel mRNA in normal and clonal (GH3) 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 (t1/2 approximately 0.5 hr) in GH3 cells. Immunoblots indicate that the steroid also increases the expression of the 76 kd Kv1.5 protein approximately 3-fold within 12 hr without altering its half-life (t1/2 approximately 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.
糖皮质激素可特异性增加正常大鼠垂体细胞和克隆（GH3）大鼠垂体细胞中Kv1.5钾通道的信使核糖核酸。在此，我们证明，糖皮质激素激动剂地塞米松可快速诱导Kv1.5基因转录，但不影响GH3细胞中Kv1.5信使核糖核酸的周转（半衰期约0.5小时）。免疫印迹表明，该类固醇在12小时内还可使76kd的Kv1.5蛋白表达增加约3倍，而不改变其半衰期（半衰期约4小时）。相比之下，Kv1.4蛋白表达不受影响。最后，我们发现Kv1.5蛋白的诱导与电压门控钾电流的非失活成分增加有关。我们的结果表明，激素和神经递质可能在数小时内通过控制钾通道基因表达来调节兴奋性。
