The authors declare that they have no competing interests.
JZ participated in the study design, performed the experiments, and drafted the manuscript. MC performed the statistical analysis and helped draft the manuscript. XW participated in the study design and provided technical support for the experiments. YC participated in the study design and critical revision of the study. WL provided technical and material support. YL participated in the conception and design of the study and the critical revision of the manuscript and supervise the experiments. All authors read and approved the final manuscript.
Detrusor overactivity (DO) secondary to partial bladder outlet obstruction (PBOO) is closely associated with alteration of ion channels. The objective of this study is to investigate the expression of the TWIK-related arachidonic acid-activated K+ channel (TRAAK) in the L6-S1 spinal cord of DO rats after PBOO.
Female Sprague–Dawley rats undergoing PBOO surgery were screened for DO by cystometry. Sham-operated rats served as controls. The expression of TRAAK in the L6-S1 spinal cord was detected by real-time polymerase chain reaction, western blotting and immunohistochemistry.
DO was successfully induced after chronic PBOO in rats, with an incidence rate of 62.5 %. Compared with sham-operated rats, the expression of TRAAK in the L6-S1 spinal cord of DO rats was significantly increased at the mRNA (1.886 ± 0.710 versus 0.790 ± 0.679, P < 0.05) and protein level (0.510 ± 0.087 versus 0.255 ± 0.107, P < 0.05). Immunohistochemical staining showed increased expression of TRAAK in the dorsal horn and ventral horn of the spinal cord.
Upregulation of TRAAK was observed in the spinal cord of DO rats after chronic PBOO, which may exert a protective effect against DO by suppressing the excitability of neurons.
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- Enhanced expression of TWIK-related arachidonic acid-activated K+ channel in the spinal cord of detrusor overactivity rats after partial bladder outlet obstruction
- BioMed Central
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