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

doi:10.1016/j.neuint.2006.09.002

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

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39 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 language	English (US)
Pages (from-to)	345-350
Number of pages	6
Journal	Neurochemistry International
Volume	50
Issue number	2
DOIs	https://doi.org/10.1016/j.neuint.2006.09.002
State	Published - 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

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10.1016/j.neuint.2006.09.002

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@article{4a4bd41ba58d4773ae37396cef621711,

title = "Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats",

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.",

keywords = "ATP, Cholinergic, Microdialysis, Purinergic, Spinal cord injury, Urinary bladder, Urothelium",

author = "Salas, {Nilson A.} and Somogyi, {George T.} and Gangitano, {David A.} and Boone, {Timothy B.} and Smith, {Christopher P.}",

note = "Funding Information: This study was supported by the National Institute of Health RO1 DK 069988 (for GTS) and The Scott Department of Urology Neurourology Fund.",

year = "2007",

month = jan,

doi = "10.1016/j.neuint.2006.09.002",

language = "English (US)",

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T1 - Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats

AU - Salas, Nilson A.

AU - Somogyi, George T.

AU - Gangitano, David A.

AU - Boone, Timothy B.

AU - Smith, Christopher P.

N1 - Funding Information: This study was supported by the National Institute of Health RO1 DK 069988 (for GTS) and The Scott Department of Urology Neurourology Fund.

PY - 2007/1

Y1 - 2007/1

N2 - 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.

AB - 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.

KW - ATP

KW - Cholinergic

KW - Microdialysis

KW - Purinergic

KW - Spinal cord injury

KW - Urinary bladder

KW - Urothelium

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

Abstract

Keywords

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