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Related Experiment Video

Updated: Mar 18, 2026

An In-vitro Preparation of Isolated Enteric Neurons and Glia from the Myenteric Plexus of the Adult Mouse
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Enteric Inhibitory Neurotransmission, Starting Down Under.

Kenton M Sanders1

  • 1Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV, 89511, USA. ksanders@medicine.nevada.edu.

Advances in Experimental Medicine and Biology
|July 6, 2016
PubMed
Summary

Enteric inhibitory neurotransmission involves non-cholinergic, non-adrenergic (NANC) pathways. Recent findings highlight purinergic signaling via P2Y1 receptors and beta-nicotinamide adenine dinucleotide (β-NAD) as key mediators in the gut.

Keywords:
Gastrointestinal motilityNitric oxidePurinesSIP syncytiumVIP

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Area of Science:

  • Gastroenterology
  • Neuroscience
  • Pharmacology

Background:

  • Enteric inhibitory neurotransmission was initially termed non-cholinergic, non-adrenergic (NANC) due to its resistance to classical neurotransmitter antagonists.
  • Adenosine triphosphate (ATP) was initially proposed as a major NANC neurotransmitter, with evidence from purine release and effects on gut preparations.
  • Small-conductance Ca(2+)-activated K(+) (SK) channels were implicated in purinergic inhibitory junction potentials (IJPs).

Purpose of the Study:

  • To review the historical development and recent advancements in understanding enteric inhibitory neurotransmission.
  • To identify the key mediators and cellular components involved in NANC signaling within the gastrointestinal tract.
  • To discuss the roles of purinergic signaling and novel neurotransmitter candidates in gut motility regulation.

Main Methods:

  • Review of historical studies and literature on enteric neurotransmission.
  • Analysis of experimental evidence implicating purines, nitric oxide (NO), and other molecules in inhibitory neurotransmission.
  • Examination of genetic models (e.g., P2Y1(-/-) mice) and cellular studies identifying signaling pathways and cell types.

Main Results:

  • Enteric inhibitory neurotransmission is mediated by multiple components, including nitric oxide (NO) and purinergic signaling.
  • The purinergic component is primarily mediated by P2Y1 receptors, as evidenced by its absence in knockout models.
  • Beta-nicotinamide adenine dinucleotide (β-NAD) or its metabolite ADP-ribose (ADPR) may be more suitable candidates for the purinergic inhibitory neurotransmitter than ATP.
  • Two distinct interstitial cell populations, Interstitial cells of Cajal and PDGFRα(+) cells, are involved in transducing NANC signals to smooth muscle cells, forming the SIP syncytium.

Conclusions:

  • Enteric inhibitory neurotransmission is a complex process involving multiple neurotransmitters and cellular signaling pathways.
  • Purinergic signaling, mediated by P2Y1 receptors and potentially β-NAD/ADPR, plays a significant role alongside NO.
  • The SIP syncytium, comprising smooth muscle and specific interstitial cells, integrates these signals for effective gut motility control.