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Neural mechanisms underlying migrating motor complex formation in mouse isolated colon.
S M Brierley1, K Nichols, D J Grasby
1Department of Physiology, University of Adelaide, Adelaide, South Australia, Australia.
British Journal of Pharmacology
|February 13, 2001
Summary
Endogenous tachykinins (TKs) and acetylcholine (ACh) play key roles in mouse colonic migrating motor complexes (MMCs). TKs mediate long-duration contractions via NK1/NK2 receptors, with nitric oxide and ATP also involved.
Area of Science:
- Gastroenterology
- Neurogastroenterology
- Colonic Motility
Background:
- Migrating motor complexes (MMCs) are crucial for gut motility.
- Intrinsic enteric reflex pathways governing MMC formation are not fully understood.
- Acetylcholine (ACh) mediates the rapid MMC component, but a non-cholinergic pathway exists.
Purpose of the Study:
- To investigate the role of endogenous tachykinins (TKs) in colonic MMC formation.
- To elucidate the relative contributions of excitatory and inhibitory pathways in MMC generation.
Main Methods:
- MMCs were recorded from mouse colon circular muscle using force transducers at four sites.
- Tachykinin (NK1 and NK2) receptor antagonists (SR-140 333, SR-48 968) were used.
- Neuronal nitric oxide synthase inhibitor (L-NOARG), apamin, and suramin were applied.
Main Results:
- Tachykinin receptor antagonists reduced MMC amplitude, abolishing long-duration contractions.
- Nitric oxide synthase inhibition affected MMC amplitude differentially across colon regions.
- Inhibitory pathway modulators (apamin, suramin) altered MMC amplitude, suggesting a role in formation regulation.
Conclusions:
- Tachykinins, ACh, nitric oxide, and ATP are integral to mouse colonic MMC neural mechanisms.
- TKs mediate the long-duration MMC component via NK1 and NK2 receptors.
- Inhibitory pathways appear to regulate MMC formation and propagation.