Anterior pituitary corticotroph cells are an integral component of the hypothalamic-pituitary-adrenal (HPA) axis which governs the physiological stress response. In response to a stressor, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) from the hypothalamus stimulate adrenocorticotrophic hormone (ACTH) release from corticotrophs. ACTH, in turn, releases glucocorticoids from the adrenal gland which negatively feedback to inhibit ACTH secretion. Corticotroph cells are electrically excitable and fire single-spike action potentials as well as showing complex bursting patterns. The aim of this project was to establish whether glucocorticoid negative feedback changes the electrical properties of murine corticotroph cells. Corticotrophs were acutely isolated 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). Stimulation with physiological concentrations of CRH and AVP (0.2nM and 2nM respectively) results in an increase in firing frequency and a transition from single spikes to bursting-like behaviour. Cells pre-treated for 1.5 hours with corticosterone (100nM) were significantly (p < 0.01) hyperpolarised compared with controls (-62.9 ±2.2mV) under basal conditions (n = 8). Although CRH and AVP could depolarise resting membrane potential in corticosterone treated cells, this was still significantly (p < 0.05) hyperpolarised (-55.7 ±2.6mV) compared with controls treated with CRH and AVP. Basal firing rate was lower in cells treated for 1.5 hours (0.12 ±0.1Hz) and although CRH/AVP was still able to increase firing frequency (0.49 ±0.13Hz), it was significantly (p < 0.05) reduced compared with control cells exposed to CRH and AVP. Furthermore, in corticosterone pre-treated cells, CRH and AVP failed to induce a significant transition from single spikes to bursting behaviour. To summarise, treatment of corticotrophs with corticosterone causes an overall suppression of both spontaneous and CRH/AVP-evoked firing frequency. Interestingly, corticosterone treated cells fail to transition from single spike to complex bursting patterns. This highlights a potential mechanism for corticosterone negative feedback although molecular targets remain to be defined.