Urine Voiding Pattern Analysis in MPTP Mouse Model of Parkinson’s Disease

Authors

  • Nipaporn Konthapakdee
  • Nusaib Sa-ih
  • Dania Cheaha
  • Ekkasit Kumarnsit

Keywords:

MPTP, Parkinson’s disease, urinary incontinence, voiding behavior, voiding spot analysis (VSA)

Abstract

Urinary bladder dysfunction, e.g., urinary frequency, urgency, and incontinence, is one of common nonmotor symptoms of patients with Parkinson’s disease (PD). 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is widely used to induce Parkinson’s disease-like in animal models. However, it remains elusive whether this model reflects urinary bladder dysfunction in PD patients. This study aims to investigate the urine voiding pattern of MPTP-induced Parkinson’s disease-like in mice using spontaneous voiding spot analysis (VSA). Male ICR mice (8 weeks old) were injected with MPTP (10 mg/kg in normal saline, i.p.) once a day for 5 consecutive days, while the control group received normal saline. Voiding pattern was investigated at day 21 after the last treatment. Filter paper and metal wire mesh were placed in the cages to determine urine pattern of the animals for 4 hours with free access to food and water. Thereafter, the urine-stained filter paper was visualized under UV light and imaged. Urine spot number, urine volume, number of small and large urine spots, percentage of volume in the center and corner were quantified. MPTP-treated mice had a significant increase in total urine spot number (control, 8.20 ± 3.0, vs MPTP, 20.40 ± 3.73, P < 0.05, Student’s unpaired t-test; n = 5 in each group) and number of small spots compared to control (control, 4.60 ± 2.62 vs MPTP, 14.80 ± 3.09, P < 0.05, Student’s unpaired t-test; n = 5 each). There was no significant difference in total urine volume, number of large urine spots, and percentage volume in the center and corner of the cages. Our findings suggest that MPTP-induced Parkinsonian-like symptoms in mice could potentially be used as a model to investigate bladder dysfunction in Parkinson’s disease.

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Author Biographies

Nipaporn Konthapakdee

Department of Physiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90112, Thailand.

Nusaib Sa-ih

Graduate Progr am in Physiology, Department of Physiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90112, Thailand.

Department of Biology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90112, Thailand.

Dania Cheaha

Department of Biology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90112, Thailand.

Research Unit for EEG Biomarkers of Neuronal diseases, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90112, Thailand.

Ekkasit Kumarnsit

Department of Physiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90112, Thailand.

Research Unit for EEG Biomarkers of Neuronal diseases, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90112, Thailand.

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Published

2019-05-07

Issue

Section

Original Articles