Chronic spinal cord injury causes upregulation of serotonin (5-HT) and 5-HT receptors in lumbosacral cord motoneurons.

Objectives: To investigate whether the voiding dysfunction caused by spinal cord injury (SCI) in rats can be improved by i.v. administration of the serotonin (5-HT) receptor agonist 2,5-dimethoxy-4-iodophenyl-2-aminopropanehydrochloride (DOI), and to discuss whether the mechanism can be ascribed to 5-HT and 5-HT receptor upregulation in lumbosacral cord motoneurons.

Materials And Methods: Female Sprague-Dawley rats were divided into two groups (SCI group vs normal control [NC] group). Under urethane anaesthesia, cystometry was performed to examine the variation in urodynamic variables before and after successive intrathecal (i.t.) administration of various doses of DOI into the lumbosacral cord. Changes in 5-HT and - receptors in the lumbosacral cord were also investigated using immunohistochemical staining and Western blot analysis.

Results: Compared with NC rats, the SCI rats had higher bladder capacity and post-void residual urine volume, and lower voiding efficiency. After SCI, DOI improved voiding efficiency, probably via external urethral sphincter (EUS) activity. Immunohistochemical staining and Western blot analysis showed that 5-HT and - receptors were upregulated in lumbosacral cord motoneurons.

Conclusion: In rats with SCI, DOI can improve voiding efficiency; this may be attributable to 5-HT and - receptor upregulation in lumbosacral cord motoneurons controlling EUS activity.