Active bicarbonate-dependent secretion evoked by 5-hydroxytryptamine in porcine ileal mucosa is mediated by opioid-sensitive enteric neurons

Benedict T. Green; David R. Brown

doi:10.1016/S0014-2999(02)02249-5

Active bicarbonate-dependent secretion evoked by 5-hydroxytryptamine in porcine ileal mucosa is mediated by opioid-sensitive enteric neurons

Benedict T. Green, David R. Brown

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

5-Hydroxytryptamine (5-HT) mediates intestinal hypersecretion associated with infection and inflammation. We tested the hypothesis that 5-HT-induced anion secretion is mediated by an opioid-sensitive enteric neural circuit. 5-HT, at a contraluminal concentration of 10 μM, increased short-circuit current by 58±7 μA/cm² in sheets of porcine ileal mucosa with attached inner submucosal plexus. Responses to 5-HT were inhibited by saxitoxin or indomethacin, and reduced in tissues bathed in Cl^-- or HCO₃^--deficient media. 5-HT action was attenuated by saxitoxin in tissues bathed in Cl^--free media, but not HCO₃-free media. The δ-opioid receptor agonist [D-Pen^2,5]enkephalin (0.1 μM) blunted the 5-HT change in short-circuit current by a mechanism sensitive to the δ-opioid receptor antagonist naltrindole. The inhibitory actions of [D-Pen^2,5]enkephalin and saxitoxin were not additive. These results suggest that 5-HT stimulates HCO₃^--dependent ion transport through a mechanism involving prostanoids and an enteric neural pathway modulated by opioids.

Original language	English (US)
Pages (from-to)	185-190
Number of pages	6
Journal	European Journal of Pharmacology
Volume	451
Issue number	2
DOIs	https://doi.org/10.1016/S0014-2999(02)02249-5
State	Published - Sep 13 2002

Bibliographical note

Funding Information:
The authors thank Dr. Scott M. O'Grady (Department of Animal Science-Physiology, University of Minnesota) for expert technical advice during the execution of this project. This study was funded in part by NIH/NIDA grant R01 DA-10200. B.T.G. was a predoctoral trainee supported by ADAMHA/NIDA Psychoneuroimmunology and Substance Abuse training grant T32 DA07239.

Keywords

Bicarbonate-dependent secretion
Cannabinoid
Enkephalin
Inflammatory mediator
Prostanoid

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10.1016/S0014-2999(02)02249-5

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title = "Active bicarbonate-dependent secretion evoked by 5-hydroxytryptamine in porcine ileal mucosa is mediated by opioid-sensitive enteric neurons",

abstract = "5-Hydroxytryptamine (5-HT) mediates intestinal hypersecretion associated with infection and inflammation. We tested the hypothesis that 5-HT-induced anion secretion is mediated by an opioid-sensitive enteric neural circuit. 5-HT, at a contraluminal concentration of 10 μM, increased short-circuit current by 58±7 μA/cm2 in sheets of porcine ileal mucosa with attached inner submucosal plexus. Responses to 5-HT were inhibited by saxitoxin or indomethacin, and reduced in tissues bathed in Cl-- or HCO3--deficient media. 5-HT action was attenuated by saxitoxin in tissues bathed in Cl--free media, but not HCO3-free media. The δ-opioid receptor agonist [D-Pen2,5]enkephalin (0.1 μM) blunted the 5-HT change in short-circuit current by a mechanism sensitive to the δ-opioid receptor antagonist naltrindole. The inhibitory actions of [D-Pen2,5]enkephalin and saxitoxin were not additive. These results suggest that 5-HT stimulates HCO3--dependent ion transport through a mechanism involving prostanoids and an enteric neural pathway modulated by opioids.",

keywords = "Bicarbonate-dependent secretion, Cannabinoid, Enkephalin, Inflammatory mediator, Prostanoid",

author = "Green, {Benedict T.} and Brown, {David R.}",

note = "Funding Information: The authors thank Dr. Scott M. O'Grady (Department of Animal Science-Physiology, University of Minnesota) for expert technical advice during the execution of this project. This study was funded in part by NIH/NIDA grant R01 DA-10200. B.T.G. was a predoctoral trainee supported by ADAMHA/NIDA Psychoneuroimmunology and Substance Abuse training grant T32 DA07239.",

year = "2002",

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doi = "10.1016/S0014-2999(02)02249-5",

language = "English (US)",

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AU - Green, Benedict T.

AU - Brown, David R.

N1 - Funding Information: The authors thank Dr. Scott M. O'Grady (Department of Animal Science-Physiology, University of Minnesota) for expert technical advice during the execution of this project. This study was funded in part by NIH/NIDA grant R01 DA-10200. B.T.G. was a predoctoral trainee supported by ADAMHA/NIDA Psychoneuroimmunology and Substance Abuse training grant T32 DA07239.

PY - 2002/9/13

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N2 - 5-Hydroxytryptamine (5-HT) mediates intestinal hypersecretion associated with infection and inflammation. We tested the hypothesis that 5-HT-induced anion secretion is mediated by an opioid-sensitive enteric neural circuit. 5-HT, at a contraluminal concentration of 10 μM, increased short-circuit current by 58±7 μA/cm2 in sheets of porcine ileal mucosa with attached inner submucosal plexus. Responses to 5-HT were inhibited by saxitoxin or indomethacin, and reduced in tissues bathed in Cl-- or HCO3--deficient media. 5-HT action was attenuated by saxitoxin in tissues bathed in Cl--free media, but not HCO3-free media. The δ-opioid receptor agonist [D-Pen2,5]enkephalin (0.1 μM) blunted the 5-HT change in short-circuit current by a mechanism sensitive to the δ-opioid receptor antagonist naltrindole. The inhibitory actions of [D-Pen2,5]enkephalin and saxitoxin were not additive. These results suggest that 5-HT stimulates HCO3--dependent ion transport through a mechanism involving prostanoids and an enteric neural pathway modulated by opioids.

AB - 5-Hydroxytryptamine (5-HT) mediates intestinal hypersecretion associated with infection and inflammation. We tested the hypothesis that 5-HT-induced anion secretion is mediated by an opioid-sensitive enteric neural circuit. 5-HT, at a contraluminal concentration of 10 μM, increased short-circuit current by 58±7 μA/cm2 in sheets of porcine ileal mucosa with attached inner submucosal plexus. Responses to 5-HT were inhibited by saxitoxin or indomethacin, and reduced in tissues bathed in Cl-- or HCO3--deficient media. 5-HT action was attenuated by saxitoxin in tissues bathed in Cl--free media, but not HCO3-free media. The δ-opioid receptor agonist [D-Pen2,5]enkephalin (0.1 μM) blunted the 5-HT change in short-circuit current by a mechanism sensitive to the δ-opioid receptor antagonist naltrindole. The inhibitory actions of [D-Pen2,5]enkephalin and saxitoxin were not additive. These results suggest that 5-HT stimulates HCO3--dependent ion transport through a mechanism involving prostanoids and an enteric neural pathway modulated by opioids.

KW - Bicarbonate-dependent secretion

KW - Cannabinoid

KW - Enkephalin

KW - Inflammatory mediator

KW - Prostanoid

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ER -

Active bicarbonate-dependent secretion evoked by 5-hydroxytryptamine in porcine ileal mucosa is mediated by opioid-sensitive enteric neurons

Abstract

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Keywords

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