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Non-neuronal release of ACh plays a key role in secretory response to luminal propionate in rat colon

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Title: Non-neuronal release of ACh plays a key role in secretory response to luminal propionate in rat colon
Authors: Yajima, Takaji Browse this author
Inoue, Ryo Browse this author
Matsumoto, Megumi Browse this author
Yajima, Masako Browse this author
Keywords: ACh
short chain fatty acid
Issue Date: 15-Feb-2011
Publisher: Blackwell Publishing
Journal Title: The Journal of Physiology
Volume: 589
Issue: 4
Start Page: 953
End Page: 962
Publisher DOI: 10.1113/jphysiol.2010.199976
Abstract: Colonic chloride secretion is induced by chemical stimuli via the enteric nervous reflex. We have previously demonstrated that propionate stimulates chloride secretion via sensory and cholinergic systems of the mucosa in rat distal colon. In this study, we demonstrate non-neuronal release of ACh in the secretory response to propionate using an Ussing chamber. Mucosa preparations from the colon, not including the myenteric and submucosal plexuses, were used. Luminal addition of propionate and serosal addition of ACh caused biphasic changes in short-circuit current (Isc). TTX (1 μM) had no effects, while atropine (10 μM) significantly inhibited the Isc response to propionate and abolished that to ACh. In response to luminal propionate stimulation, ACh was released into serosal fluid. A linear relationship was observed between the maximal increase in Isc and the amounts of ACh released 5 min after propionate stimulation. This ACh releases induced by propionate was not affected by atropine and bumetanide, although both drugs significantly reduced the Isc responses to propionate. Luminal addition of 3-Cl-propionate, an inactive analogue of propionate, abolished both ACh release and Isc response produced by propionate. RT-PCR analysis indicated that isolated crypt cells from the distal colon expressed an enzyme of ACh synthesis (ChAT) and transporters of organic cation (OCTs), but not neuronal CHT1 and VAChT. The isolated crypt cells contained comparable amounts of ACh to the residual muscle tissues including nerve plexuses. In conclusion, the non-neuronal release of ACh from colonocytes coupled with propionate stimulation plays a key role in chloride secretion, via the paracrine action of ACh on muscarinic receptors of colonocytes.
Rights: The definitive version is available at and
Type: article (author version)
Appears in Collections:創成研究機構 (Creative Research Institution) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 矢島 高二

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