Increased Expression of TREK-1 K+ Channel in the Dorsal Root Ganglion of Rats with Detrusor Overactivity After Partial Bladder Outlet Obstruction.

BACKGROUND Changes in expression and activity of ion channels are important pathophysiological mechanisms underlying detrusor overactivity (DO) in partial bladder outlet obstruction (PBOO). The objective of this study was to examine the expression of TREK-1 channel in the bladder and central nervous system of DO rats. MATERIAL AND METHODS Thirty Sprague-Dawley rats were subjected to PBOO operations and those displaying non-voiding contractions (NVCs) in cystometry were classified as DO. Sham-operated rats without NVCs in cystometry served as controls. The expression and distribution of TREK-1 in the bladder, spinal cord, and dorsal root ganglion (DRG) were detected by real time-PCR, western blot, and immunohistochemistry. RESULTS TREK-1 channel expression in the DRG was significantly increased at the mRNA level (11.20±3.762 vs. 3.209±1.505, P<0.01) and protein level (2.195±0.058 vs. 1.713±0.066, P<0.01) in DO rats as compared to control rats. However, the expression of TREK-1 mRNA in the bladder (1.380±0.810 vs. 4.206±3.827, P>0.05) and spinal cord (0.764±0.357 vs. 0.696±0.188, P>0.05) was comparable between the 2 groups. Immunohistochemistry showed enhanced immunoreactive signals of TREK-1 channel in the DRG, but not in the spinal cord and bladder. CONCLUSIONS TREK-1 channel was upregulated in the DRG of DO rats after chronic PBOO, which might suppress neuronal excitability and play a protective role in bladder overactivity in PBOO.