Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats

Nilson A. Salas, George T. Somogyi, David A. Gangitano, Timothy B. Boone, Christopher P. Smith

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

Neurally intact (NI) rats and chronic spinal cord injured (SCI) rats were studied to determine how activation of mechanosensory or cholinergic receptors in the bladder urothelium evokes ATP release from afferent terminals in the bladder as well as in the spinal cord. Spinal cord transection was performed at the T9-T10 level 2-3 weeks prior to the experiment and a microdialysis fiber was inserted in the L6-S1 lumbosacral spinal cord one day before the experiments. Mechanically evoked (i.e. 10 cm/W bladder pressure) ATP release into the bladder lumen was approximately 6.5-fold higher in SCI compared to NI rats (p < 0.05). Intravesical carbachol (CCh) induced a significantly greater release of ATP in the bladder from SCI as compared to NI rats (3424.32 ± 1255.57 pmol/ml versus 613.74 ± 470.44 pmol/ml, respectively, p < 0.05). However, ATP release in NI or SCI rats to intravesical CCh was not affected by the muscarinic antagonist atropine (Atr). Spinal release of ATP to bladder stimulation with 10 cm/W pressure was five-fold higher in SCI compared to NI rats (p < 0.05). CCh also induced a significantly greater release of spinal ATP in SCI rats compared to controls (4.3 ± 0.9 pmol versus 0.90 ± 0.15 pmol, p < 0.05). Surprisingly, the percent inhibitory effect of Atr on CCh-induced ATP release was less pronounced in SCI as compared to NI rats (49% versus 89%, respectively). SCI induces a dramatic increase in intravesical pressure and cholinergic receptor evoked bladder and spinal ATP release. Muscarinic receptors do not mediate intravesical CCh-induced ATP release into the bladder lumen in NI or SCI rats. In NI rats sensory muscarinic receptors are the predominant mechanism by which CCh induces ATP release from primary afferents within the lumbosacral spinal cord. Following SCI, however, nicotinic or purinergic receptor mechanisms become active, as evidenced by the fact that Atr was only partially effective in inhibiting CCh-induced spinal ATP release.

Original languageEnglish (US)
Pages (from-to)345-350
Number of pages6
JournalNeurochemistry International
Volume50
Issue number2
DOIs
StatePublished - Jan 2007

Keywords

  • ATP
  • Cholinergic
  • Microdialysis
  • Purinergic
  • Spinal cord injury
  • Urinary bladder
  • Urothelium

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

Fingerprint Dive into the research topics of 'Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats'. Together they form a unique fingerprint.

Cite this