ArticleNeurogastroenterology and motility2013
Differential release of β-NAD(+) and ATP upon activation of enteric motor neurons in primate and murine colons.
Article in Neurogastroenterology and motility, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
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- Neurotransmitters responsible for purinergic motor neurotransmission and regulation of GI motility.Autonomic neuroscience : basic & clinical · 2021Article
- Extracellular metabolism of the enteric inhibitory neurotransmitter β-nicotinamide adenine dinucleotide (β-NAD) in the murine colon.The Journal of physiology · 2020Article
- Optogenetic analysis of neuromuscular transmission in the colon of ChAT-ChR2-YFP BAC transgenic mice.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
- Loss of nitric oxide-mediated inhibition of purine neurotransmitter release in the colon in the absence of interstitial cells of Cajal.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Post-inflammatory Ileitis Induces Non-neuronal Purinergic Signaling Adjustments of Cholinergic Neurotransmission in the Myenteric Plexus.Frontiers in pharmacology · 2017Article
- Urothelial purine release during filling of murine and primate bladders.American journal of physiology. Renal physiology · 2016Article
- A commonly used ecto-ATPase inhibitor, ARL-67156, blocks degradation of ADP more than the degradation of ATP in murine colon.Neurogastroenterology and motility · 2016Article
- Enteric Inhibitory Neurotransmission, Starting Down Under.Advances in experimental medicine and biology · 2016Review
- Appropriate experimental approach is critical for identifying neurotransmitter substances: application to enteric purinergic neurotransmission.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Response to Mutafova-Yambolieva and Sanders.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- β-Nicotinamide adenine dinucleotide acts at prejunctional adenosine A1 receptors to suppress inhibitory musculomotor neurotransmission in guinea pig colon and human jejunum.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Uridine adenosine tetraphosphate is a novel neurogenic P2Y1 receptor activator in the gut.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The purinergic neurotransmitter revisited: a single substance or multiple players?Pharmacology & therapeutics · 2014Review
- Purinergic neuromuscular transmission in the gastrointestinal tract; functional basis for future clinical and pharmacological studies.British journal of pharmacology · 2014Review
- Platelet-derived growth factor receptor-α-positive cells and not smooth muscle cells mediate purinergic hyperpolarization in murine colonic muscles.American journal of physiology. Cell physiology · 2014Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe purinergic component of enteric inhibitory neurotransmission is important for normal motility in the gastrointestinal (GI) tract. Controversies exist about the purine(s) responsible for inhibitory responses in GI muscles: ATP has been assumed to be the purinergic neurotransmitter released from enteric inhibitory motor neurons; however, recent studies demonstrate that β-nicotinamide adenine dinucleotide (β-NAD(+)) and ADP-ribose mimic the inhibitory neurotransmitter better than ATP in primate and murine colons. The study was designed to clarify the sources of purines in colons of Cynomolgus monkeys and C57BL/6 mice.
methodsHigh-performance liquid chromatography with fluorescence detection was used to analyze purines released by stimulation of nicotinic acetylcholine receptors (nAChR) and serotonergic 5-HT(3) receptors (5-HT(3)R), known to be present on cell bodies and dendrites of neurons within the myenteric plexus. KEY
resultsNicotinic acetylcholine receptor or 5-HT(3)R agonists increased overflow of ATP and β-NAD(+) from tunica muscularis of monkey and murine colon. The agonists did not release purines from circular muscles of monkey colon lacking myenteric ganglia. Agonist-evoked overflow of β-NAD(+), but not ATP, was inhibited by tetrodotoxin (0.5 μmol L(-1)) or ω-conotoxin GVIA (50 nmol L(-1)), suggesting that β-NAD(+) release requires nerve action potentials and junctional mechanisms known to be critical for neurotransmission. ATP was likely released from nerve cell bodies in myenteric ganglia and not from nerve terminals of motor neurons. CONCLUSIONS & INFERENCES: These results support the conclusion that ATP is not a motor neurotransmitter in the colon and are consistent with the hypothesis that β-NAD(+), or its metabolites, serve as the purinergic inhibitory neurotransmitter.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.