Selective up-regulation of NMDA-NRI receptor expression in myenteric plexus after TNBS induced colitis in rats

QiQi Zhou, Robert M. Caudle, Donald D. Price, Arseima Y. Del Valle-Pinero, G. Nicholas Verne

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Background: N-methyl-D-aspartic acid (NMDA) spinal cord receptors play an important role in the development of hyperalgesia following inflammation. It is unclear, however, if changes in NMDA subunit receptor gene expression in the colonic myenteric plexus are associated with colonic inflammation. We investigated regulation of NMDA-NRI receptor gene expression in TNBS induced colitis in rats. Male Sprague-Dawley rats (150 g-250 g) were treated with 20 mg trinitrobenzene sulfonic acid (TNBS) diluted in 50% ethanol. The agents were delivered with a 24 gauge catheter inserted into the lumen of the colon. The animals were sacrificed at 2, 7, 14, 21, and 28 days after induction of the colitis, their descending colon was retrieved for reverse transcription-polymerase chain reaction; a subset of animals' distal colon was used for two-dimensional (2-D) western analysis and immunocytochemistry. Results: NRI-exon 5 (N1) and NRI-exon 21 (C1) appeared 14, 21 and 28 days after TNBS treatment. NRI pan mRNA was up-regulated at 14, 21, and 28 days. The NRI -exon 22 (C2) mRNA did not show significant changes. Using 2-D western analysis, untreated control rats were found to express only NRI001 whereas TNBS treated rats expressed NRI001, NRI011, and NRI111. Immunocytochemistry demonstrated NRI-N1 and NRI-C1 to be present in the myenteric plexus of TNBS treated rats. Conclusion: These results suggest a role for colonic myenteric plexus NMDA receptors in the development of neuronal plasticity and visceral hypersensitivity in the colon. Up-regulation of NMDA receptor subunits may reflect part of the basis for chronic visceral hypersensitivity in conditions such as post-infectious irritable bowel syndrome.

Original languageEnglish (US)
Article number3
JournalMolecular Pain
Volume2
DOIs
StatePublished - Jan 17 2006

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Trinitrobenzenes
Myenteric Plexus
Sulfonic Acids
N-Methylaspartate
Colitis
Up-Regulation
Exons
Colon
Hypersensitivity
Immunohistochemistry
Inflammation
Descending Colon
Gene Expression
Messenger RNA
Neuronal Plasticity
Irritable Bowel Syndrome
Hyperalgesia
Reverse Transcription
Sprague Dawley Rats
Spinal Cord

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Molecular Medicine
  • Cellular and Molecular Neuroscience

Cite this

Selective up-regulation of NMDA-NRI receptor expression in myenteric plexus after TNBS induced colitis in rats. / Zhou, QiQi; Caudle, Robert M.; Price, Donald D.; Del Valle-Pinero, Arseima Y.; Verne, G. Nicholas.

In: Molecular Pain, Vol. 2, 3, 17.01.2006.

Research output: Contribution to journalArticle

Zhou, QiQi ; Caudle, Robert M. ; Price, Donald D. ; Del Valle-Pinero, Arseima Y. ; Verne, G. Nicholas. / Selective up-regulation of NMDA-NRI receptor expression in myenteric plexus after TNBS induced colitis in rats. In: Molecular Pain. 2006 ; Vol. 2.
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abstract = "Background: N-methyl-D-aspartic acid (NMDA) spinal cord receptors play an important role in the development of hyperalgesia following inflammation. It is unclear, however, if changes in NMDA subunit receptor gene expression in the colonic myenteric plexus are associated with colonic inflammation. We investigated regulation of NMDA-NRI receptor gene expression in TNBS induced colitis in rats. Male Sprague-Dawley rats (150 g-250 g) were treated with 20 mg trinitrobenzene sulfonic acid (TNBS) diluted in 50{\%} ethanol. The agents were delivered with a 24 gauge catheter inserted into the lumen of the colon. The animals were sacrificed at 2, 7, 14, 21, and 28 days after induction of the colitis, their descending colon was retrieved for reverse transcription-polymerase chain reaction; a subset of animals' distal colon was used for two-dimensional (2-D) western analysis and immunocytochemistry. Results: NRI-exon 5 (N1) and NRI-exon 21 (C1) appeared 14, 21 and 28 days after TNBS treatment. NRI pan mRNA was up-regulated at 14, 21, and 28 days. The NRI -exon 22 (C2) mRNA did not show significant changes. Using 2-D western analysis, untreated control rats were found to express only NRI001 whereas TNBS treated rats expressed NRI001, NRI011, and NRI111. Immunocytochemistry demonstrated NRI-N1 and NRI-C1 to be present in the myenteric plexus of TNBS treated rats. Conclusion: These results suggest a role for colonic myenteric plexus NMDA receptors in the development of neuronal plasticity and visceral hypersensitivity in the colon. Up-regulation of NMDA receptor subunits may reflect part of the basis for chronic visceral hypersensitivity in conditions such as post-infectious irritable bowel syndrome.",
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AB - Background: N-methyl-D-aspartic acid (NMDA) spinal cord receptors play an important role in the development of hyperalgesia following inflammation. It is unclear, however, if changes in NMDA subunit receptor gene expression in the colonic myenteric plexus are associated with colonic inflammation. We investigated regulation of NMDA-NRI receptor gene expression in TNBS induced colitis in rats. Male Sprague-Dawley rats (150 g-250 g) were treated with 20 mg trinitrobenzene sulfonic acid (TNBS) diluted in 50% ethanol. The agents were delivered with a 24 gauge catheter inserted into the lumen of the colon. The animals were sacrificed at 2, 7, 14, 21, and 28 days after induction of the colitis, their descending colon was retrieved for reverse transcription-polymerase chain reaction; a subset of animals' distal colon was used for two-dimensional (2-D) western analysis and immunocytochemistry. Results: NRI-exon 5 (N1) and NRI-exon 21 (C1) appeared 14, 21 and 28 days after TNBS treatment. NRI pan mRNA was up-regulated at 14, 21, and 28 days. The NRI -exon 22 (C2) mRNA did not show significant changes. Using 2-D western analysis, untreated control rats were found to express only NRI001 whereas TNBS treated rats expressed NRI001, NRI011, and NRI111. Immunocytochemistry demonstrated NRI-N1 and NRI-C1 to be present in the myenteric plexus of TNBS treated rats. Conclusion: These results suggest a role for colonic myenteric plexus NMDA receptors in the development of neuronal plasticity and visceral hypersensitivity in the colon. Up-regulation of NMDA receptor subunits may reflect part of the basis for chronic visceral hypersensitivity in conditions such as post-infectious irritable bowel syndrome.

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