AB75. Lower urinary tract dysfunction in a pink1 gene knockout rat model for Parkinson’s disease

Bladder dysfunction is a common non-motor disorder on Parkinson’s disease (PD) patients. A new transgenic Pink1 gene knockout rat model of PD has been developed recently. To explore lower urinary tract function in this newly established PD model and provide possible therapeutic base for PD urinary complications. Twelve Pink1 KO rats (pink1-/-, LEH-pink1tm 1sage, 40 weeks old) and twelve wide type rats (pink1+/+, LEH, 40 weeks old) were used in this project. After acclimation, the rats underwent 24 hours metabolic cage test, conscious cystometry, and leak point pressure test. Their bladders were harvested, weighted and then fixed for histological study. Total volume, micturition times, and voided volume per micturition were calculated for 24h metabolic cage test. Pressure parameters, micturition frequency, bladder capacity/compliance, volume parameters, leak point pressure (LPP) were analyzed according to the result of cystometry and LPP test. Body weight, bladder weight, and the general pathologic changes in bladder were also checked. Continuous variables were compared between groups using t-test. Categorical variables were compared using Chi-square test. P<0.05 was set as statistical significant. Pink1 KO rats acquired the functional disorder of detrusor over activity compared to wild type rats. Hyperplasia of smooth muscle and nerves were noted in the bladder wall of Pink1 KO rats. More specific nerve changes and specific causality among dopaminergic neuron loss, pathologic alterations of bladder, and functional changes should be investigated in the future. Pink1-/- rat model of PD exhibited bladder dysfunction at the age of 40 weeks old. Detrusor over activity was the main change. Smooth muscle and nerves in bladder wall displayed the alteration of hyperplasia. This is a better transgenic rat model of PD induced detrusor over activity for future study.