ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2010
Mounting evidence against the role of ICC in neurotransmission to smooth muscle in the gut.
Review in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- Contribution of neuroligin and neurexin alternative splicing to the establishment of enteric neuronal synaptic specificity.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- CaPhysiological reviews · 2024Review
- Calcium transients in intramuscular interstitial cells of Cajal of the murine gastric fundus and their regulation by neuroeffector transmission.The Journal of physiology · 2022Article
- LEtS set the tone.The Journal of physiology · 2022Article
- Functional circuits and signal processing in the enteric nervous system.Cellular and molecular life sciences : CMLS · 2020Review
- Enteric nervous system: sensory transduction, neural circuits and gastrointestinal motility.Nature reviews. Gastroenterology & hepatology · 2020Review
- Spontaneous Electrical Activity and Rhythmicity in Gastrointestinal Smooth Muscles.Advances in experimental medicine and biology · 2019Review
- The role of Ano1 in mediating cholinergic neurotransmission in the murine gastric fundus.The Journal of physiology · 2018Article
- The cells and conductance mediating cholinergic neurotransmission in the murine proximal stomach.The Journal of physiology · 2018Article
- Stem Cell Factor/Kit Signal Insufficiency Contributes to Hypoxia-Induced Intestinal Motility Dysfunctions in Neonatal Mice.Digestive diseases and sciences · 2017Article
- Analysis of spatiotemporal pattern and quantification of gastrointestinal slow waves caused by anticholinergic drugs.Organogenesis · 2017Article
- Inhibitory responses mediated by vagal nerve stimulation are diminished in stomachs of mice with reduced intramuscular interstitial cells of Cajal.Scientific reports · 2017Article
- Convergence of inhibitory neural inputs regulate motor activity in the murine and monkey stomach.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Insights into the mechanisms underlying colonic motor patterns.The Journal of physiology · 2016Review
- CrossTalk proposal: Interstitial cells are involved and physiologically important in neuromuscular transmission in the gut.The Journal of physiology · 2016Article
- CrossTalk opposing view: Interstitial cells are not involved and physiologically important in neuromuscular transmission in the gut.The Journal of physiology · 2016Article
- Dominant role of interstitial cells of Cajal in nitrergic relaxation of murine lower oesophageal sphincter.The Journal of physiology · 2015Article
- 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
- Interstitial cells: regulators of smooth muscle function.Physiological reviews · 2014Review
- Responses to enteric motor neurons in the gastric fundus of mice with reduced intramuscular interstitial cells of cajal.Journal of neurogastroenterology and motility · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
How nerves transmit their signals to regulate activity of smooth muscle is of fundamental importance to autonomic and enteric physiology, clinical medicine, and therapeutics. A traditional view of neurotransmission to smooth muscles has been that motor nerve varicosities release neurotransmitters that act on receptors on smooth muscles to cause their contraction or relaxation via electromechanical and pharmacomechanical signaling pathways in the smooth muscle. In recent years, an old hypothesis that certain interstitial cells of Cajal (ICC) may transduce neural signals to smooth muscle cells has been resurrected. This later hypothesis is based on indirect evidence of closer proximity and presence of synapses between the nerve varicosities and ICC, gap junctions between ICC and smooth muscles, and presence of receptors and signaling pathways for the neurotransmitters and ICC. This indirect evidence is at best circumstantial. The direct evidence is based on the reports of loss of neurotransmission in mutant animals lacking ICC due to c-Kit receptor deficiency. However, a critical analysis of the recent data show that animals lacking ICC have normal cholinergic and purinergic neurotransmission and tachykinergic neurotransmission is actually increased. The status of nitrergic neurotransmission in c-Kit deficient animals has been controversial. However, reports suggest that 1) nitrergic neurotransmission in the internal anal sphincter does not require ICC and 2) the in vivo phenotype of ICC deficiency does not resemble nNOS deficiency. 3) The most recent report, in this issue of the Journal, concludes that impaired nitrergic neurotransmission may be due to smooth muscle defects associated with c-Kit receptor deficiency.
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What OpenQuestion holds
Registered trials
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.