ArticleThe Journal of physiology2012
Adenosine 5-diphosphate-ribose is a neural regulator in primate and murine large intestine along with β-NAD(+).
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 51 citations in OpenAlex.
- Disruption of gastrointestinal PDGFRαAmerican journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells.Biomolecules · 2024Review
- Review
- Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner.Metabolites · 2022Article
- Mechanosensitive Hydrolysis of ATP and ADP in Lamina Propria of the Murine Bladder by Membrane-Bound and Soluble Nucleotidases.Frontiers in physiology · 2022Article
- CaAdvances in experimental medicine and biology · 2022Article
- Neurotransmitters responsible for purinergic motor neurotransmission and regulation of GI motility.Autonomic neuroscience : basic & clinical · 2021Article
- The Extracellular NADome Modulates Immune Responses.Frontiers in immunology · 2021Review
- Extracellular metabolism of the enteric inhibitory neurotransmitter β-nicotinamide adenine dinucleotide (β-NAD) in the murine colon.The Journal of physiology · 2020Article
- NAMPT and NAPRT: Two Metabolic Enzymes With Key Roles in Inflammation.Frontiers in oncology · 2020Review
- An ex vivo bladder model with detrusor smooth muscle removed to analyse biologically active mediators released from the suburothelium.The Journal of physiology · 2019Article
- Comparison of inhibitory neuromuscular transmission in the Cynomolgus monkey IAS and rectum: special emphasis on differences in purinergic transmission.The Journal of physiology · 2018Article
- 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
- 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
- Signaling mechanism for modulation by ATP of glycine receptors on rat retinal ganglion cells.Scientific reports · 2016Article
- Enteric Inhibitory Neurotransmission, Starting Down Under.Advances in experimental medicine and biology · 2016Review
- Nudix hydrolases degrade protein-conjugated ADP-ribose.Scientific reports · 2015Article
- Appropriate experimental approach is critical for identifying neurotransmitter substances: application to enteric purinergic neurotransmission.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Neuropharmacology of purinergic receptors in human submucous plexus: Involvement of P2X₁, P2X₂, P2X₃ channels, P2Y and A₃ metabotropic receptors in neurotransmission.Neuropharmacology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Adenosine 5′-triphosphate (ATP) has long been considered to be the purine inhibitory neurotransmitter in gastrointestinal (GI) muscles, but recent studies indicate that another purine nucleotide, β-nicotinamide adenine dinucleotide (β-NAD(+)), meets pre- and postsynaptic criteria for a neurotransmitter better than ATP in primate and murine colons. Using a small-volume superfusion assay and HPLC with fluorescence detection and intracellular microelectrode techniques we compared β-NAD(+) and ATP metabolism and postjunctional effects of the primary extracellular metabolites of β-NAD(+) and ATP, namely ADP-ribose (ADPR) and ADP in colonic muscles from cynomolgus monkeys and wild-type (CD38(+/+)) and CD38(−/−) mice. ADPR and ADP caused membrane hyperpolarization that, like nerve-evoked inhibitory junctional potentials (IJPs), were inhibited by apamin. IJPs and hyperpolarization responses to ADPR, but not ADP, were inhibited by the P2Y1 receptor antagonist (1R,2S,4S,5S)-4-[2-iodo-6-(methylamino)-9H-purin-9-yl]-2-(phosphonooxy)bicyclo[3.1.0]hexane-1-methanol dihydrogen phosphate ester tetraammonium salt (MRS2500). Degradation of β-NAD(+) and ADPR was greater per unit mass in muscles containing only nerve processes than in muscles also containing myenteric ganglia. Thus, mechanisms for generation of ADPR from β-NAD(+) and for termination of the action of ADPR are likely to be present near sites of neurotransmitter release. Degradation of β-NAD(+) to ADPR and other metabolites appears to be mediated by pathways besides CD38, the main NAD-glycohydrolase in mammals. Degradation of β-NAD(+) and ATP were equal in colon. ADPR like its precursor, β-NAD(+), mimicked the effects of the endogenous purine neurotransmitter in primate and murine colons. Taken together, our observations support a novel hypothesis in which multiple purines contribute to enteric inhibitory regulation of gastrointestinal motility.
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