Abstract

The aim of this study is to investigate whether ketamine could relieve the social stress (SS)-related bladder dysfunction in mice. The FVB mice were randomly assigned to either undergo SS exposure for 60 minutes per day on seven consecutive days for 4 weeks (SS1) or control without SS (SS0). The SS0 were then allocated to single or no injection of ketamine (SS0K1 and SS0K0). In the group of SS1, the SS1 mice were allocated to receive single injection of saline (SS1K0), single dose (SS1K1) or five daily dose of (SS1K5) ketamine injection (25 mg/kg/day/ip) since day 22. In vivo cystometry and tissue bath wire myography were performed on day 29. Serum and urine level of brain-derived neurotrophic factor (BDNF) were measured with enzyme-linked immunosorbent assay. In mice without social stress exposure, ketamine administration did not significantly affect voiding frequency (P > .05). SS1 K0 , SS1 K1, and SS1 K5 had significantly lower voiding frequency than that of control (SS1 K0 ) (each n = 15, P < .05). Ketamine administration reversed the trend of decreased voiding frequency in SS1 mice. Stressed mice had significant higher serum level of BDNF that reduced by short-term ketamine. Stressed mice had detrusor overactivity and impaired detrusor contractility which were not reversed by short-term ketamine. Social stress leads to elevated serum BDNF, infrequent voiding, detrusor overactivity, and impaired contractility. Short-term administration of ketamine may improve SS-related infrequent voiding and elevated serum BDNF level. However, ketamine did not improve SS-related bladder dysfunction on urodynamic and myography studies.

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