Body weight was significantly increased (27±0.48 vs. 20±0.23 g, p<0.0001) and the uterus weight was significantly decreased (0.016±0.0011 vs. 0.076±0.0045 g, p<0.0001) in OVX vs. control mice. In CMG, there were no significant differences in CMG parameters between sham and OVX at baseline; i.e. intercontraction intervals (ICI) (540±35 vs. 550±37 s, p=0.85), peak amplitude during voiding (42±1.6 vs. 46±1.6 cmH2O, p=0.11), pressure at baseline (PB) (2.8±0.22 vs. 3.3±0.24 cmH2O, p=0.14), pressure threshold (PT) (6.5±0.32 vs. 6.0±0.25 cmH2O, p=0.26), a number of non-voiding contractions (0.20±0.0.027 vs. 0.14±0.025 /min, p=0.092), voided volume (94±5.8 vs. 90 ±5.8 µl, p=0.48), post-void residual (PVR) (2.4±1.3 vs. 3.1±1.0 µl, p=0.66), bladder capacity (96±5.8 vs. 91±5.9 µl, p=0.54), voiding efficiency (VE) (98±1.1 vs. 97±1.1 %, p=0.55), and compliance (0.045±0.016 vs. 0.037±0.0022 ml/H2O, p=0.61) (figure 1). However, OVX mice showed a significant decrease in ICI (700±100 to 270±60 s, p=0.0047), voided volume (110±16 to 50±11 µl, p=0.0041), and bladder capacity (110±16 to 50±11 µl, p=0.0041) after intravesical 0.1% AA administration, whereas 0.1% AA did not affect any CMG parameters in control mice (figure 1). Intravesical administration of 1mM amiloride blocked the effect of AA in OVX mice (figure 2). In RT-PCR, the expression of ASIC1 was significantly increased in bladder mucosa of OVX mice (p=0.00080). Furthermore, OVX mice with C-fiber desensitization by capsaicin pretreatment, intravesical 0.1% AA administration had no effect on bladder function; i.e. ICI (730±62 to 740±59 s, p=0.78), voided volume (120±6.9 to 120±7.0 µl, p=0.43) and bladder capacity (120±7.7 to 120±7.7 µl, p=0.99) although, in OVX mice with vehicle pretreatment, intravesical 0.1% AA irritation still significantly decreased ICI, voided volume, and bladder capacity.