Nerve growth factor (NGF) elicits bladder hyperactivity following acute intravesical administration and is involved in experimentally induced cystitis ⁽¹⁾, whilst 2 week intrathecal delivery of NGF⁽²⁾ or administration of NGF into the bladder wall reduces bladder capacity and increases voiding frequency in rats⁽³⁾. We investigated the duration of action of acute intravesical NGF on voiding parameters in anaesthetised cystometry, and also the effects of chronic I.P. dosing of NGF in conscious rats. Female Wistar rats (225-260g) were anaesthetised with isoflurane (2-5% in O₂) and urethane (1.25g/kg I.V.). A jugular vein (anaesthetic infusion), carotid artery (BP measurement) and trachea were cannulated. The bladder was cannulated via the urethra and tied at the external meatus, creating a closed system for isovolumetric cystometry. Following baseline cystometrograms with saline (75μl/min) until reflex bladder contractions occurred (threshold volume), the bladder was filled to capacity with 20μg/ml NGF or vehicle (10% DMSO in saline) which was held in situ for 1 hour (h) before draining. Cystometrograms were then repeated at 1, 2, 3, and 4h post treatment. In a separate study rats were anaesthetised with isoflurane, and the bladder cannulated aseptically via the urethra. The bladder was filled with 1ml of either 20μg/ml NGF or vehicle which was held in situ for 1h before draining. The catheter was removed and animals allowed to recover for 24h before undergoing anaesthetised cystometry as described above. In conscious studies rats (225-260g) were dosed daily for 10 days with 0.1mg/kg NGF or saline 10ml/kg I.P. and voiding function assessed the following morning via metaboles over 3h. Mean ± S.E.M. from each study were compared by ANOVA for NGF vs. vehicle treated rats, P<0.05 was considered statistically significant. Intravesical NGF (n=5) significantly decreased % baseline threshold volume vs. vehicle (n=4) at 2 (63.5±4.6 vs. 106.2±10.7), 3 (78.9±4.5 vs. 102.2±7.7) and 4h post treatment (75.7±7.5 vs. 108±7.4). Contraction frequency was significantly increased in the NGF treated group vs. vehicle at 1 (4±0.6 vs. 2±0.9), 2 (12±1.4 vs. 2±0.9), 3 (9±1.1 vs. 3±0.9) and 4h post-dose (10±2.1 vs. 2±0.9). At 24h post NGF there were no significant effects on either threshold volume or contraction frequency. In conscious rats an increase in voiding frequency and reduction in volume per void developed over time in the NGF treated group (n=4), reaching significance at day 5 for voiding frequency, and at day 6 for volume/void vs. vehicle (n=4). No significant difference between NGF and vehicle treatment was observed more than 24h post the last treatment day. These results indicate that depending on the mode of administration, NGF can produce both an acute and more chronic bladder hyperactivity that persists for up to 24h post dose.