Neurological insults including spinal cord injury (SCI) lead to disturbances in bladder function which include an acute areflexic phase followed by chronic bladder overactivity or underactivity. We previously investigated cellular changes in the SCI rat bladder, 5 weeks after injury and reported altered distribution of interstitial cells (IC), smooth muscle hypertrophy and patchy denervation (1). These changes were correlated with an underactive, hypercompliant phenotype (2). The purpose of the present study was to investigate structural and functional changes in the SCI rat bladder at selected time points after injury. Female Sprague Dawley rats underwent spinal cord transection at T8/T9 in accordance with the European Commission Directive of 22 September 2010 (2010/63/EU). Animals underwent in vivo cystometry under anaesthesia by subcutaneous injection of urethrane (1.2g/kg) at selected time-points post-SCI before being humanely sacrificed. Bladders were removed and processed for histology, immunofluorescence and confocal imaging. Histological and immunofluorescence studies were carried out on 4 tissue samples from at least 3 animals. Cystometry demonstrated a loss of voiding and non-voiding contractions in acute SCI bladders at 2h (N=5) and 24h (N=4). Overactivity later developed and was characterised by an increased frequency of voiding contractions from 0.43±0.1min-1 (mean±SEM) in spinal-intact animals (N=5) to 1.4±0.64min-1 (N=3; p<0.05) at 4wk, and 1.84±0.33min-1 (N=3; p<0.05, Anova, post-hoc Dunnett’s) at 8wk. Chronic SCI bladders also exhibited urinary retention/incomplete emptying. Initial loss of the urothelial layer in the acute phase was accompanied with inflammation throughout the bladder wall, which was repaired by 2wk. Notable smooth muscle hypertrophy occurred from 1wk. PDGFRα+-IC networks in the lamina propria were disrupted in the acute phase, but recovered in the later stages. PDGFRα+-IC in the detrusor were disrupted as early as 24h with marked loss of cellular morphology. This was correlated with partial denervation. In the chronic phase, the morphology of detrusor IC did not return to normal. Interestingly, α-smooth muscle actin+-myofibroblasts which were not present in controls, were detected in the bladder wall at 1wk and 2 wk post-SCI. In conclusion, the acute SCI bladder is associated with loss of voiding and non-voiding contractions along with initial disruption of lamina propria PDGFRα+-IC networks. Cellular remodelling throughout the overactive chronic phase appears to restore lamina propria IC but the detrusor layer is typified with persistent hypertrophy, patchy denervation and disrupted IC.