Colokinetic effect of noradrenaline in the spinal defecation center: implication for motility disorders

Chronic abdominal pain in irritable bowel syndrome (IBS) usually appears in combination with disturbed bowel habits, but the etiological relationship between these symptoms remains unclear. Noradrenaline is a major neurotransmitter controlling pain sensation in the spinal cord. To test the hypothesi...

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Veröffentlicht in:Scientific reports 2015-07, Vol.5 (1), p.12623-12623, Article 12623
Hauptverfasser: Naitou, Kiyotada, Shiina, Takahiko, Kato, Kurumi, Nakamori, Hiroyuki, Sano, Yuuki, Shimizu, Yasutake
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container_title Scientific reports
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Shiina, Takahiko
Kato, Kurumi
Nakamori, Hiroyuki
Sano, Yuuki
Shimizu, Yasutake
description Chronic abdominal pain in irritable bowel syndrome (IBS) usually appears in combination with disturbed bowel habits, but the etiological relationship between these symptoms remains unclear. Noradrenaline is a major neurotransmitter controlling pain sensation in the spinal cord. To test the hypothesis that the descending noradrenergic pathway from the brain stem moderates gut motility, we examined effects of intrathecal application of noradrenaline to the spinal defecation center on colorectal motility. Colorectal intraluminal pressure and expelled volume were recorded in vivo in anesthetized rats. Intrathecal application of noradrenaline into the L6-S1 spinal cord, where the lumbosacral defecation center is located, caused propulsive contractions of the colorectum. Inactivation of spinal neurons by tetrodotoxin blocked the effect of noradrenaline. Pharmacological experiments showed that the effect of noradrenaline is mediated primarily by alpha-1 adrenoceptors. The enhancement of colorectal motility by intrathecal noradrenaline was abolished by severing of the pelvic nerves. Our results demonstrate that noradrenaline acting on sacral parasympathetic preganglionic neurons through alpha-1 adrenoceptors causes propulsive motility of the colorectum in rats. Considering that visceral pain activates the descending inhibitory pathways including noradrenergic neurons, our results provide a rational explanation of the concurrent appearance of chronic abdominal pain and colonic motility disorders in IBS patients.
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Noradrenaline is a major neurotransmitter controlling pain sensation in the spinal cord. To test the hypothesis that the descending noradrenergic pathway from the brain stem moderates gut motility, we examined effects of intrathecal application of noradrenaline to the spinal defecation center on colorectal motility. Colorectal intraluminal pressure and expelled volume were recorded in vivo in anesthetized rats. Intrathecal application of noradrenaline into the L6-S1 spinal cord, where the lumbosacral defecation center is located, caused propulsive contractions of the colorectum. Inactivation of spinal neurons by tetrodotoxin blocked the effect of noradrenaline. Pharmacological experiments showed that the effect of noradrenaline is mediated primarily by alpha-1 adrenoceptors. The enhancement of colorectal motility by intrathecal noradrenaline was abolished by severing of the pelvic nerves. Our results demonstrate that noradrenaline acting on sacral parasympathetic preganglionic neurons through alpha-1 adrenoceptors causes propulsive motility of the colorectum in rats. 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Noradrenaline is a major neurotransmitter controlling pain sensation in the spinal cord. To test the hypothesis that the descending noradrenergic pathway from the brain stem moderates gut motility, we examined effects of intrathecal application of noradrenaline to the spinal defecation center on colorectal motility. Colorectal intraluminal pressure and expelled volume were recorded in vivo in anesthetized rats. Intrathecal application of noradrenaline into the L6-S1 spinal cord, where the lumbosacral defecation center is located, caused propulsive contractions of the colorectum. Inactivation of spinal neurons by tetrodotoxin blocked the effect of noradrenaline. Pharmacological experiments showed that the effect of noradrenaline is mediated primarily by alpha-1 adrenoceptors. The enhancement of colorectal motility by intrathecal noradrenaline was abolished by severing of the pelvic nerves. 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subjects 631/443/376
692/617/375/1824
Adrenergic alpha-1 Receptor Antagonists - pharmacology
Adrenergic alpha-Agonists - administration & dosage
Adrenergic alpha-Agonists - pharmacology
Anesthetics, Local - pharmacology
Animals
Brain stem
Colon - drug effects
Colon - innervation
Colon - physiology
Defecation
Defecation - drug effects
Defecation - physiology
Gastric motility
Gastrointestinal Motility - drug effects
Gastrointestinal Motility - physiology
Humanities and Social Sciences
Hypogastric Plexus - physiopathology
Hypogastric Plexus - surgery
Inactivation
Injections, Spinal
Intestine
Irritable bowel syndrome
Kinetics
Lumbosacral Region
Male
Motility
multidisciplinary
Nerves
Neurons
Norepinephrine
Norepinephrine - administration & dosage
Norepinephrine - pharmacology
Pain
Pain perception
Parasympathetic nervous system
Pelvis
Prazosin - pharmacology
Rats, Sprague-Dawley
Rectum - drug effects
Rectum - innervation
Rectum - physiology
Rodents
Sacrum
Science
Spinal cord
Spinal Cord - drug effects
Spinal Cord - physiology
Tetrodotoxin
Tetrodotoxin - pharmacology
title Colokinetic effect of noradrenaline in the spinal defecation center: implication for motility disorders
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