The control of electrical excitability of anterior pituitary corticotrophs is essential for coordinating the release of stress hormones in response to stress. A variety of ion channels are reported to be important for controlling corticotroph excitability however potassium channels that regulate spontaneous and secretagogue-evoked (CRH and AVP) activity, remain poorly understood. In several pituitary cells, members of ether-a-go-go related (Erg, Kv11.x) family of voltage dependent potassium channels control both spontaneous and hormone-induced regulation of excitability. In these studies, we used a pharmacological approach to test the role of Erg channels in both basal and CRH/AVP evoked excitability.  Corticotrophs from male BK-POMC-GFP mice on a C57BL6 background (age 2-5 months), were isolated and maintained in primary culture in accordance with UK Home office requirements. Current clamp and voltage- clamp recordings were performed using the perforated patch clamp approach with protocols controlled by Clampex and analysed using Clampfit. Pharmacological inhibition of Erg currents were conducted by bath exposure to E-4031 (5 µM), a selective pharmacological inhibitor of Erg channels or vehicle control using a gravity perfusion system. Statistical analysis was performed using Mixed effect analysis ANOVA with further analysis by Sidak’s and Tukey’s multiple comparison tests with Mean ± SD.  E-4031 (n=9) significantly increased basal spike frequency (from 0.1 ± 0.2 Hz to 1.5 ± 1.0 Hz; p< 0.05).  This E-4031-induced increase in basal spike frequency resulted in an apparent significant (p<0.01) attenuation of the normal CRH/AVP evoked fold increase in spike frequency (CRH/AVP alone increased spike frequency 14.9 ± 6.2 fold but in the presence of E4031 the fold increase in CRH/AVP-induced spike frequency was only 2.0 ± 0.9 fold). E4031 also significantly reduced the normal CRH/AVP evoked transition to bursting activity in comparison to the vehicle control (n=7) treated corticotrophs (burstiness factor in presence of CRH/AVP was reduced from 0.4 ± 0.3 to 0.1 ± 0.1 (p< 0.01) and event duration from 206.9 ± 188.2 to 58 ± 45.9 ms (p< 0.01) in the presence of E4031). E-4031 did not change the spike amplitude or the resting membrane potential under basal or CRH/AVP treated conditions compared to the vehicle control. In voltage clamp recordings E-4031 sensitive currents were routinely recorded but the amplitude was highly variable between cells.  CRH/AVP (n=6) had no significant effect on isolated Erg currents suggesting they are not a direct target for intracellular pathways activated by CRH/AVP in corticotrophs. RNA sequencing of FACS-purified corticotrophs from male POMC-GFP mice revealed highest expression of Erg 1 with a lower expression level of Erg 2 & Erg 3. Our data reveal that while Erg channels are expressed in murine male corticotrophs and play a role in controlling basal and CRH/AVP evoked activity they are not direct targets for regulation of corticotroph excitability by CRH/AVP. Further studies are required to understand the role of Erg currents in controlling corticotroph physiology.