| First Author | Hirdes W | Year | 2010 |
| Journal | Endocrinology | Volume | 151 |
| Issue | 3 | Pages | 1079-88 |
| PubMed ID | 20068004 | Mgi Jnum | J:168523 |
| Mgi Id | MGI:4888480 | Doi | 10.1210/en.2009-0718 |
| Citation | Hirdes W, et al. (2010) Gonadotropin-releasing hormone inhibits ether-a-go-go-related gene K+ currents in mouse gonadotropes. Endocrinology 151(3):1079-88 |
| abstractText | Secretion of LH from gonadotropes is initiated by a GnRH-induced increase in intracellular Ca(2+) concentration ([Ca(2+)](i)). This increase in [Ca(2+)](i) is the result of Ca(2+) release from intracellular stores and Ca(2+) influx through voltage-dependent Ca(2+) channels. Here we describe an ether-a-go-go-related gene (erg) K(+) current in primary mouse gonadotropes and its possible function in the control of Ca(2+) influx. To detect gonadotropes, we used a knock-in mouse strain, in which GnRH receptor-expressing cells are fluorescently labeled. Erg K(+) currents were recorded in 80-90% of gonadotropes. Blockage of erg currents by E-4031 depolarized the resting potential by 5-8 mV and led to an increase in [Ca(2+)](i), which was abolished by nifedipine. GnRH inhibited erg currents by a reduction of the maximal erg current and in some cells additionally by a shift of the activation curve to more positive potentials. In conclusion, the erg current contributes to the maintenance of the resting potential in gonadotropes, thereby securing a low [Ca(2+)](i) by restricting Ca(2+) influx. In addition, the erg channels are modulated by GnRH by an as-yet unknown signal cascade. |
