Lower urinary tract symptoms (LUTS) become prevalent with aging and affect millions; however, therapy is often ineffective because etiology is unknown. Existing assays of LUT function in animal models are often invasive, however a non-invasive assay is required to study symptom progression and determine genetic correlates. Here we present a spontaneous voiding assay which is simple, reproducible, quantitative and non-invasive. Young females from eight strains of inbred mice - 129S1/SvImJ, A/J, C57BL/6J, NOD/ShiLtJ, NZO/H1LtJ, CAST/EiJ, PWK/PhJ, and WSB/EiJ - were tested for urination patterns on filter paper. Repeat testing at different times of the day showed minimal within individual and within strain variation, but all parameters (spot number, total volume, percentage area in primary void, corner voiding and center voiding) exhibited significant variation between strains. Calculation of the intraclass correlation coefficient, an estimate of broad sense heritability (H2), for each time of day and for each voiding parameter, revealed highly significant heritability (spot number, 61%; percentage urine in primary void, 90%; total volume, 94% [afternoon data]). Cystometrograms confirmed strong strain-specific urodynamic characteristics. Behavior/voiding correlation analysis showed no correlation with anxiety phenotypes. Diagnostically, the assay revealed LUTS in several systems, including demonstration of voiding abnormalities in older C57BL/6J mice (18-24 months), in a model of protamine sulfate induced urothelial damage and in a model of sucrose-induced diuresis. This assay may be used to derive pathophysiological LUT readouts from mouse models. Voiding characteristics are heritable traits, opening the way for genetic studies of LUTS using outbred mouse populations.