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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

BACKGROUND: 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 co...

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Detalles Bibliográficos
Autores principales: Zhang, Junlong, Cao, Mingxin, Wu, Xilian, Chen, Yu, Liang, Weijie, Liang, Yueyou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4596457/
https://www.ncbi.nlm.nih.gov/pubmed/26444419
http://dx.doi.org/10.1186/s12894-015-0092-8
Descripción
Sumario:BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.