In humans and many socialised animals voiding can be suppressed, even when the bladder is full, until the individual finds itself in a safe and socially acceptable environment. Failure of this inhibitory control mechanism may underlie some forms of urinary urge incontinence. Afferent signals from the distended bladder activate a spino-midbrain-spinal pathway that initiates co-ordinated activation of the detrusor and external urethral sphincter (EUS) to induce voiding [1]. Critical synaptic relays are present in the caudalmost part of the ventrolateral periaqueductal grey matter (cvlatPAG) [2]. In humans deep brain stimulation (DBS) is increasingly used to manipulate the activity of brain circuits for therapeutic gain [3]. We have investigated whether DBS in the cvlatPAG can suppress voiding in rats. Urethane anaesthetised (1.5g Kg-1 ip) male Sprague Dawley rats (n=13, 259-403g) were instrumented to record femoral arterial pressure, bladder pressure, EMG from the EUS and urine output. The trachea was cannulated and a venous catheter inserted to administer fluids. Rectal temperature was maintained at 36.5-37.5°C. A needle connected to a t-piece was inserted into the bladder to measure bladder pressure and infuse saline (6ml h-1, 165mM), which induced cycles of filling and voiding (0.41±0.05min-1 mean±S.E.M). Each void was accompanied by a sharp rise in bladder pressure and the development of bursting activity in the EUS. An insulated stainless steel stimulating electrode, tip 60μm, was positioned stereotaxically in the caudal midbrain. The cvlatPAG and underlying ventral tegmental area were mapped using a standard stimulus (0.5ms, 60Hz, 180μA for 20s), which was applied within 2s of the onset of the sharp rise in bladder pressure that indicated an imminent void. Stimulation sites were verified histologically from marks of electrode tracks in fixed brain tissue. At 34/72 sites tested, voiding was attenuated (n=19) or completely suppressed (n=15) during the stimulation period. Urine output was reduced from 7.3±0.6 to 1.4±0.3 drops, the accompanying rise in bladder pressure reduced from 19.6±0.8 to 15.0±0.2 mmHg (P<0.05 Student’s paired T-test) and bursting activity in the EUS failed to develop. Stimulation at effective sites was accompanied by a modest pressor response (15.6±1.3 mmHg) and tachycardia (17.9±2.6 beats min-1). Effective stimulation sites were localised within the ventral half of the caudal PAG at approximately P8.8 [4] and extended into the underlying tegmental field. At 9 effective sites we investigated the effect of longer periods of continuous stimulation (1-7 min). We were able to suppress voiding completely for up to 7.3 min, despite the continued infusion of saline into the bladder. Our data show that even when the bladder is full, micturition can be deferred by using DBS to modulate activity in the micturition reflex pathway at the level of the cvlatPAG.