Tachykinergic neurotransmission is enhanced in duodenum from dystrophic (mdx) mice

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Abstract

1 Duodenal longitudinal muscle of mdx mice, an animal model for Duchenne muscular dystrophy, showed a decrease in the electrically evoked nonadrenergic, noncholinergic (NANC) inhibitory responses associated with a reduction of the participation of nitric oxide (NO). In this study, we investigated whether the impairment of NO could also lead to alterations in the NANC excitatory transmission. 2 Nerve-evoked responses consisted of an inhibitory phase followed, at the end of stimulation, by an excitatory response characterised by an increase in amplitude of the spontaneous contractions. In mdx mice, the amplitude of the nerve-evoked contractions was significantly higher than in normals. 3 N(omega)-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, increased the amplitude of the nerve-evoked contractions only in normals, being ineffective in mdx mice. Apamin, a blocker of Ca(2+)-dependent potassium channels, failed to affect the nerve-evoked contractions. 4 In both models, substance P and neurokinin A produced concentration-dependent contractions, reduced by tachykinin NK(1) and NK(2) receptor antagonists, respectively. Moreover, NK(1) and NK(2) receptor antagonists reduced the amplitude of the nerve-evoked contractions. 5 Sodium nitroprusside (SNP) reduced the amplitude of nerve-evoked contractions similarly in normal and mdx mice. ODQ, but not apamin, prevented the SNP-induced effects. SNP did not affect the contractions induced by exogenous tachykinins. 6 The results suggest that NO can exert an inhibitory modulatory role on tachykinergic excitatory transmission via activation of guanylyl cyclase in mouse duodenum. In mdx mice, the impairment of NO function leads to an increase in the nerve-evoked contractions.
Lingua originaleEnglish
pagine (da-a)334-341
Numero di pagine8
RivistaBritish Journal of Pharmacology
Volume145
Stato di pubblicazionePublished - 2005

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Inbred mdx Mouse
Duodenum
Synaptic Transmission
Nitric Oxide
Nitroprusside
Neurokinin-2 Receptors
Apamin
Tachykinins
NG-Nitroarginine Methyl Ester
Neurokinin A
Duchenne Muscular Dystrophy
Guanylate Cyclase
Potassium Channels
Substance P
Animal Models
Muscles

All Science Journal Classification (ASJC) codes

  • Pharmacology

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title = "Tachykinergic neurotransmission is enhanced in duodenum from dystrophic (mdx) mice",
abstract = "1 Duodenal longitudinal muscle of mdx mice, an animal model for Duchenne muscular dystrophy, showed a decrease in the electrically evoked nonadrenergic, noncholinergic (NANC) inhibitory responses associated with a reduction of the participation of nitric oxide (NO). In this study, we investigated whether the impairment of NO could also lead to alterations in the NANC excitatory transmission. 2 Nerve-evoked responses consisted of an inhibitory phase followed, at the end of stimulation, by an excitatory response characterised by an increase in amplitude of the spontaneous contractions. In mdx mice, the amplitude of the nerve-evoked contractions was significantly higher than in normals. 3 N(omega)-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, increased the amplitude of the nerve-evoked contractions only in normals, being ineffective in mdx mice. Apamin, a blocker of Ca(2+)-dependent potassium channels, failed to affect the nerve-evoked contractions. 4 In both models, substance P and neurokinin A produced concentration-dependent contractions, reduced by tachykinin NK(1) and NK(2) receptor antagonists, respectively. Moreover, NK(1) and NK(2) receptor antagonists reduced the amplitude of the nerve-evoked contractions. 5 Sodium nitroprusside (SNP) reduced the amplitude of nerve-evoked contractions similarly in normal and mdx mice. ODQ, but not apamin, prevented the SNP-induced effects. SNP did not affect the contractions induced by exogenous tachykinins. 6 The results suggest that NO can exert an inhibitory modulatory role on tachykinergic excitatory transmission via activation of guanylyl cyclase in mouse duodenum. In mdx mice, the impairment of NO function leads to an increase in the nerve-evoked contractions.",
author = "Flavia Mule' and Zizzo, {Maria Grazia} and Serio, {Rosa Maria}",
year = "2005",
language = "English",
volume = "145",
pages = "334--341",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
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TY - JOUR

T1 - Tachykinergic neurotransmission is enhanced in duodenum from dystrophic (mdx) mice

AU - Mule', Flavia

AU - Zizzo, Maria Grazia

AU - Serio, Rosa Maria

PY - 2005

Y1 - 2005

N2 - 1 Duodenal longitudinal muscle of mdx mice, an animal model for Duchenne muscular dystrophy, showed a decrease in the electrically evoked nonadrenergic, noncholinergic (NANC) inhibitory responses associated with a reduction of the participation of nitric oxide (NO). In this study, we investigated whether the impairment of NO could also lead to alterations in the NANC excitatory transmission. 2 Nerve-evoked responses consisted of an inhibitory phase followed, at the end of stimulation, by an excitatory response characterised by an increase in amplitude of the spontaneous contractions. In mdx mice, the amplitude of the nerve-evoked contractions was significantly higher than in normals. 3 N(omega)-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, increased the amplitude of the nerve-evoked contractions only in normals, being ineffective in mdx mice. Apamin, a blocker of Ca(2+)-dependent potassium channels, failed to affect the nerve-evoked contractions. 4 In both models, substance P and neurokinin A produced concentration-dependent contractions, reduced by tachykinin NK(1) and NK(2) receptor antagonists, respectively. Moreover, NK(1) and NK(2) receptor antagonists reduced the amplitude of the nerve-evoked contractions. 5 Sodium nitroprusside (SNP) reduced the amplitude of nerve-evoked contractions similarly in normal and mdx mice. ODQ, but not apamin, prevented the SNP-induced effects. SNP did not affect the contractions induced by exogenous tachykinins. 6 The results suggest that NO can exert an inhibitory modulatory role on tachykinergic excitatory transmission via activation of guanylyl cyclase in mouse duodenum. In mdx mice, the impairment of NO function leads to an increase in the nerve-evoked contractions.

AB - 1 Duodenal longitudinal muscle of mdx mice, an animal model for Duchenne muscular dystrophy, showed a decrease in the electrically evoked nonadrenergic, noncholinergic (NANC) inhibitory responses associated with a reduction of the participation of nitric oxide (NO). In this study, we investigated whether the impairment of NO could also lead to alterations in the NANC excitatory transmission. 2 Nerve-evoked responses consisted of an inhibitory phase followed, at the end of stimulation, by an excitatory response characterised by an increase in amplitude of the spontaneous contractions. In mdx mice, the amplitude of the nerve-evoked contractions was significantly higher than in normals. 3 N(omega)-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, increased the amplitude of the nerve-evoked contractions only in normals, being ineffective in mdx mice. Apamin, a blocker of Ca(2+)-dependent potassium channels, failed to affect the nerve-evoked contractions. 4 In both models, substance P and neurokinin A produced concentration-dependent contractions, reduced by tachykinin NK(1) and NK(2) receptor antagonists, respectively. Moreover, NK(1) and NK(2) receptor antagonists reduced the amplitude of the nerve-evoked contractions. 5 Sodium nitroprusside (SNP) reduced the amplitude of nerve-evoked contractions similarly in normal and mdx mice. ODQ, but not apamin, prevented the SNP-induced effects. SNP did not affect the contractions induced by exogenous tachykinins. 6 The results suggest that NO can exert an inhibitory modulatory role on tachykinergic excitatory transmission via activation of guanylyl cyclase in mouse duodenum. In mdx mice, the impairment of NO function leads to an increase in the nerve-evoked contractions.

UR - http://hdl.handle.net/10447/23649

M3 - Article

VL - 145

SP - 334

EP - 341

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

ER -