2005 Fiscal Year Final Research Report Summary
The role of acetylcholine and muscarinic receptor on rat bladder during storage phase.
| Project/Area Number |
16591608
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
AIKAWA Ken Fukushima Medical University, School of Medicine, Assistant professor, 医学部, 講師 (80295419)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Yasukuni Fukushima Medical University, School of Medicine, Assistant professor, 医学部, 講師 (50220744)
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| Project Period (FY) |
2004 – 2005
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| Keywords | bladder urothelium / acetylcholine / muscarinic receptor / anticholinergic drug / bladder afferent / storage symptom / c-Fos / rat |
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| Research Abstract |
It was confirmed using immunohistologic method with the anti-ChAT (acetylcholine synthesis enzyme) antibody (AB144P, Chemicon) that acetylcholine synthesis enzyme existed in the rat bladder urothelium. The expression of ChAT revealed no difference among normal, ovariectomized and obstructed rat bladders. The subtype 1, 2, 3 and 5 of muscarinic receptor also existed in the rat bladder urothelium. In regard to the expression of these receptors, there was no difference among normal, ovariectomized and obstructed rat bladders. We studied whether acetylcholine and muscarinic receptor alter the storage function through an afferent activation from the bladder. The c-Fos expression in L6 spinal cord is able to use as a marker for afferent neuronal activation induced by bladder irritation in rat. Therefore, we investigated the number of c-Fos positive cells in L6 spinal cord and cystometric parameters among control, anticholinergic drug or cholinesterase inhibitor administrated rats. Oxybutynin acted on the afferent pathway because oxybutynin inhibited spinal c-Fos expression without affecting voiding contraction. And this reduction of the afferent input results in the increased bladder capacity and extended micturition interval. Furthermore, major action site of acetylcholine is also the afferent pathway during storage phase because the inhibition of acetylcholine resolution with edrophonium increased the afferent pathway activation without affecting voiding contraction. This increase of the afferent input resulted in the decreased bladder capacity and shortened micturition interval. These findings suggest that acetylcholine through muscarinic receptor play an important role as a transmitter for non-nociceptive stimulus from the bladder during storage phase.
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