GnRH induces hormone secretion from gonadotropes by an increase in the cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i), predominantly due to release of Ca²⁺ from intracellular stores. We asked the question to which degree an influx of Ca²⁺ through the plasma membrane may contribute to the increase in [Ca²⁺]_i. One candidate ion channel which could be involved in such an effect is the erg (ether-à-go-go-related gene) K⁺ channel. Here we show that erg K⁺ currents can be recorded in gonadotropes from male adult mice in acute pituitary slices and culture. Gonadotropes were identified by using a knock-in mouse, in which gonadotropes are fluorescent by expression of YFP (Wen et al. 2008, Endocrinology 149: 2701). Single-cell RT-PCR revealed transcripts for erg1a and erg2 subunits. The resting potential of about -50 mV was depolarized by about 5 mV by 1 mM E-4031, a substance known to specifically block erg channels. Ca²⁺ imaging showed that E-4031 induced a slow increase in the fluorescence ratio by 10% (in 3 mM extracellular [K⁺]) or 23% (in 8 mM extracellular [K⁺]). The increase in [Ca²⁺]_i following application of E-4031 was blocked by nifedipine, prohibiting the influx of external Ca²⁺ through voltage-dependent L-type Ca²⁺ channels. GnRH caused a 30% increase in the fluorescence ratio (in 8 mM K⁺). The increases in [Ca²⁺]_i, induced by GnRH and by E-4031 were additive. 1 nM GnRH reduced the maximal erg current amplitude by 34% and shifted the midpoint of the activation curve by 11 mV to more depolarized potentials. These GnRH-induced effects on the erg current in gonadotropes resembled those induced by TRH on erg currents in lactotropes (Bauer & Schwarz 2001, J Membr Biol, 182:1). Our data indicate that erg currents contribute to the maintenance of the resting potential in gonadotropes and that their inhibition by GnRH induces a depolarization and activation of Ca²⁺ channels. The subsequent influx of Ca²⁺ may contribute to secretion of LH and FSH.