In the heart, ether-à-go-go-related gene (erg) K⁺ channels mediates the rapidly activating component of the delayed rectifying K current (I_Kr), which contributes to repolarization of the myocardial action potential. Non-functioning of I_Kr leads to one form of the Long-QT-syndrome. Erg channels are also prominently expressed in the pituitary. Previously we have described the presence and function of erg currents in lactotropes. In these cells blockage of erg channels is an important step in inducing the 2nd phase of the TRH-mediated increase in prolactin secretion (reviewed by Bauer and Schwarz, 2001). We have now done experiments on a new mouse model which allows visualization and manipulation of gonadotrope cells. Using gene targeting in embryonic stem cells we generated mice in which Cre recombinase is coexpressed with the gonadotropin-releasing hormone (GnRH) receptor, which is expressed in gonadotrope cells. More than 99% of gonadotropin containing cells were labeled by YFP fluorescence and readily identifiable in dissociated pituitary cell culture allowing potentially unbiased sampling from the gonadotrope population. About 50% of gonadotropes do not exhibit secretion of luteinizing hormone (LH) or follicle-stimulating hormone (FSH). We also show that gonadotropes respond to GnRH with a broad range of changes in the membrane potential as well as in [Ca²⁺]_i. Gonadotropes do also express erg channels. We show that blockage of the erg current with the specific blocker E-4031, induces a large depolarization of the gonadotrope membrane potential (16 mV in 7 cells investigated by now) and a large increase in [Ca²⁺]_i. However, this would be deviant from the current hypothesis which presumes that the large GnRH-induced increase in [Ca²⁺]_i initiating secretion is predominantly due to release of Ca²⁺ from intracellular stores. This increase in [Ca²⁺]_i occurs in the form of slow oscillations of about 0.1 Hz which can be detected electrophysiologically by oscillations of the membrane potential due to activation of small Ca²⁺ -activated K⁺ channels (SK). These slow oscillations are believed to be due to an interplay between release of Ca²⁺ from intracellular stores and reuptake of Ca²⁺ (reviewed by Stojilkovic et al., 2005, Hille et al., 1995). The influx of Ca²⁺ through voltage-dependent Ca²⁺ channels during the short action potentials seems not to be sufficient to increase the cytoplasmic [Ca²⁺].