AI Article Synopsis

  • The study aimed to investigate changes in TWIK-related arachidonic acid-activated K(+) channels in the spinal cord of rats after bladder obstruction and its effects on bladder dysfunction.
  • Female Sprague-Dawley rats underwent either complete bladder outlet obstruction or a sham procedure, with subsequent analysis of spinal cord tissue for channel expression using various techniques.
  • Findings indicated lower expression of these channels in obstructed rats, suggesting that their downregulation may contribute to increased neuronal activity and heightened bladder sensitivity, offering insights into overactive bladder conditions resulting from such obstructions.

Article Abstract

Objectives: To study the altered expression of TWIK-related arachidonic acid-activated K(+) channel in the L6-S1 spinal cord of rats after complete bladder outlet obstruction, and to investigate the role of TWIK-related arachidonic acid-activated K(+) channel in the neurogenic mechanism of bladder dysfunction.

Methods: Female Sprague-Dawley rats were randomly divided into a complete bladder outlet obstruction group and a sham-operated control group. Cystometry was carried out and tissues of L6-S1 spinal cord were obtained for detection of TWIK-related arachidonic acid-activated K(+) channel mRNA and protein by real-time polymerase chain reaction, western blot and immunohistochemistry.

Results: The bladder outlet obstruction rat model was established. Real-time polymerase chain reaction, western blot and immunohistochemistry showed that the expression of TWIK-related arachidonic acid-activated K(+) channel was lower in the L6-S1 spinal cord of the bladder outlet obstruction rats, compared with the control rats.

Conclusions: Downregulation of TWIK-related arachidonic acid-activated K(+) channel might enhance the excitability of the neurons and increase the sensitivity of the bladder, probably providing a new study model of overactive bladder secondary to bladder outlet obstruction.

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Source
http://dx.doi.org/10.1111/j.1442-2042.2012.03072.xDOI Listing

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