Urine production is reduced during sleep, largely due to absence of fluid intake and increased secretion of ADH. Functional bladder capacity also increases, enabling larger volumes of urine to be stored (Negoro et al, 2013). This effect may be centrally-mediated. Micturition is dependent on the functional integrity of a spino-midbrain-spinal loop that relays in the caudal ventrolateral periaqueductal grey (vlPAG) (Stone et al, 2011). We therefore investigated 1) whether urodynamic parameters change during alterations in brain state and 2) whether such effects involve the PAG. The urethane anaesthetised rat shows spontaneous cyclical changes in EEG waveform that are considered to reflect changes in sleep-like brain states (Clement et al, 2008). We used this preparation to make urodynamic measurements during continuous cystometry whilst recording neuronal activity in the PAG. Male urethane anaesthetised Wistar rats (1.4g Kg-1 i.p.) were instrumented to record blood pressure, heart rate, tracheal air flow and cortical EEG and for intravenous infusion of fluids. Rectal temperature was maintained at 37oC. Following a laparotomy the dome of the bladder was pierced with a needle to allow infusion of saline and simultaneous recording of bladder pressure. Bipolar electrodes were inserted into the external urethral sphincter (EUS) to record EMG. Single unit activity in the PAG was recorded using an insulated tungsten electrode. Infusion of saline into the bladder (6ml h-1) evoked repeated cycles of filling and voiding (0.3±0.02 min-1). Each void was characterized by a steep rise in bladder pressure and development of rhythmic bursting activity in the EUS. During the experiment the EEG cycled spontaneously between high amplitude low frequency (1Hz) waves (‘deactivated’ state similar to slow wave sleep) and low amplitude, high frequency activity waves (‘activated’ state similar to rapid eye movement sleep), mean period 22min. There was no detectable change in depth of anaesthesia. On transition from the ‘activated’ to ‘deactivated’ state the threshold bladder pressure for initiating a void increased from 11.2±0.6 to 14.4±0.9 SEM mmHg (p<0.01, paired t-test) accompanied by a decrease in end filling bladder compliance (0.18±0.02 to 0.11± 0.04 ml mmHg-1, p<0.05, log transformed values). Of 10 spontaneously active units in the vlPAG, which showed excitatory or inhibitory responses time locked to voiding, the basal firing rate of 7 also cycled in parallel with changes in EEG. Firing decreased from 9.8±3.2 to 2.0±1.3Hz (p<0.05) as the EEG cycled from the low amplitude ‘activated’ state to synchronized slow wave activity. All changes were reversed as the EEG cycled back to the ‘activated’ state. We suggest that the micturition reflex is reset centrally during slow wave sleep in a manner that promotes continence, via a mechanism mediated via the cvlatPAG.