Alteration of nitrergic neuromuscular transmission as a result of acute experimental colitis in rat

Tae Sik Sung, Jun-Ho La, Tae Wan Kim, Il Suk Yang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4% acetic acid in the rat. Animals were sacrificed at 4 h and 48 h post-acetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nuω-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acid-treated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.

Original languageEnglish (US)
Pages (from-to)143-150
Number of pages8
JournalJournal of Veterinary Science
Volume7
Issue number2
StatePublished - May 2006
Externally publishedYes

Fingerprint

colitis
Colitis
Acetic Acid
acetic acid
rats
nitric oxide
NADPH Dehydrogenase
Nitric Oxide
NG-Nitroarginine Methyl Ester
electric field
nitric oxide synthase
Electric Stimulation
Nitrergic Neurons
neurons
Enteric Nervous System
Myenteric Plexus
Muscles
muscles
myeloperoxidase
inflammatory bowel disease

Keywords

  • Colitis
  • Electrical field stimulation
  • N-nitro-L-arginine methyl ester
  • Neuronal nitric oxide
  • Nitrergic neuron

ASJC Scopus subject areas

  • veterinary(all)

Cite this

Alteration of nitrergic neuromuscular transmission as a result of acute experimental colitis in rat. / Sung, Tae Sik; La, Jun-Ho; Kim, Tae Wan; Yang, Il Suk.

In: Journal of Veterinary Science, Vol. 7, No. 2, 05.2006, p. 143-150.

Research output: Contribution to journalArticle

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abstract = "Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4{\%} acetic acid in the rat. Animals were sacrificed at 4 h and 48 h post-acetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nuω-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acid-treated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.",
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