Corticotroph cells from the anterior pituitary are an important component of the hypothalamic-pituitary-adrenal (HPA) axis, which controls the neuroendocrine response to stress. HPA axis dysfunction can have many consequences on health. In response to a stressor, the hypothalamic neuropeptides corticotrophin-releasing hormone (CRH) and AVP act synergistically on corticotrophs to stimulate synthesis and release of adrenocorticotrophic hormone (ACTH). Corticotroph cells are electrically excitable and fire single-spike action potentials as well as showing complex bursting patterns. There is evidence to suggest that large conductance calcium- and voltage-gated potassium (BK) channels promote bursting behaviour in multiple pituitary cell types. The aim of this project was to establish the role of BK channels in corticotroph excitability. Corticotrophs were cultured from male mice (aged 2-5 months) constitutively expressing green fluorescent protein (GFP) under control of the POMC promoter (POMC-GFP). Electrophysiological recordings were obtained using the perforated patch clamp technique in the current clamp configuration. Under basal conditions, cells had a resting membrane potential of -53.7 ±1.5mV (n = 7, Data are Means ± SEM) and showed low frequency spontaneous action potentials (0.34 ±0.14Hz). CRH and AVP (0.2nM and 2nM respectively) caused a significant (p < 0.01, ANOVA) depolarisation of the resting membrane potential to -47.4 ±0.74mV. There was also a significant (p < 0.01) increase in firing frequency from 0.34 ±0.14Hz to 0.99 ±0.27Hz. The increase in firing frequency was associated with a transition from a predominantly single-spike firing pattern to a bursting-like behaviour. To address whether BK channels control bursting activity, experiments were performed on cells treated with BK channel blocker paxilline (1μM). Bursting was quantified by calculating mean event length and mean peaks/event (burst factor, BF). While CRH/AVP significantly increased bursting in control cells, pharmacological inhibition of BK channels greatly reduced, but did not abolish bursting. The role of BK channels in promoting bursting was further investigated using cells isolated from BK knockout mice. These cells also failed to significantly transition from spiking to bursting following CRH/AVP stimulation. In summary, it can be concluded that the BK channel plays an important role in the generation of bursting behaviour in corticotroph cells. Interestingly, bursting was not completely abolished in paxilline treated or BK knockout cells. This would indicate that although the BK channel is an important component in the generation of bursting behaviour in corticotroph cells, there may be contribution from other ion channels.