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Related Experiment Videos

Substance P gene expression in acute experimental colitis.

M Reinshagen1, G Adler, V E Eysselein

  • 1Department of Medicine I, University of Ulm, Robert Kochstr. 8, 89081 Ulm, Germany.

Regulatory Peptides
|September 22, 1995
PubMed
Summary

Inflammation reduces substance P (SP) protein in the colon and dorsal root ganglia (DRG) but preserves SP gene expression, indicating neuronal integrity during colitis.

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Area of Science:

  • Neurogastroenterology
  • Inflammatory Bowel Disease Research
  • Neuropeptide Signaling

Background:

  • Previous studies indicated decreased substance P (SP) in the colon muscle layer during colitis, with SP primarily located in intrinsic neurons.
  • The reduction in SP content during inflammation could be due to decreased intrinsic SP levels or damage to SP-containing neurons.

Purpose of the Study:

  • To investigate SP gene expression in intrinsic (colon muscle) and extrinsic (dorsal root ganglia, DRG) neurons during colitis.
  • To determine if SP transcription is maintained during inflammation as an indicator of neuronal viability.

Main Methods:

  • Colitis was induced in rabbits using formalin enemas and immune complex injection.
  • SP content was measured using radioimmunoassay (RIA).

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  • SP gene expression was analyzed via Northern blot analysis in colon muscle and DRG (L4-S4).

    • Main Results:

    • Immunoreactive SP decreased by 40% in the colon muscle layer and 60% in the DRG of colitis animals compared to controls.
    • SP gene expression remained unchanged in both the colon muscle layer and DRG 48 hours after colitis induction.
    • This contrasts with the significant reduction observed in SP protein levels.

    Conclusions:

    • Preserved SP gene expression suggests that intrinsic and extrinsic SP neurons remain viable during experimental colitis.
    • The observed decrease in immunoreactive SP indicates that SP is released from both intrinsic and extrinsic neurons during inflammation.
    • This study supports the concept of neuronal release of SP as a response to inflammatory stimuli in the gut.