ArticleMolecular and cellular neurosciences2014
Caenorhabditis elegans nicotinic acetylcholine receptors are required for nociception.
Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
10 citing papers in PubMed, 26 citations in OpenAlex.
- The CRTC-1 transcriptional domain is required for COMPASS complex-mediated longevity in C. elegans.Nature aging · 2023Article
- Specific N-glycans regulate an extracellular adhesion complex during somatosensory dendrite patterning.EMBO reports · 2022Article
- TheMolecules (Basel, Switzerland) · 2022Article
- The nematode C. elegans senses airborne sound.Neuron · 2021Article
- Neuronal regulatedeLife · 2021Article
- Neurite Branching Regulated by Neuronal Cell Surface Molecules inFrontiers in neuroanatomy · 2020Review
- Mechanisms that regulate morphogenesis of a highly branched neuron in C. elegans.Developmental biology · 2019Review
- GTL-1, a Calcium Activated TRPM Channel, Enhances Nociception.Frontiers in pharmacology · 2019Article
- Expanded genetic screening ineLife · 2018Article
- Understanding Synaptogenesis and Functional Connectome in C. elegans by Imaging Technology.Frontiers in synaptic neuroscience · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Polymodal nociceptors sense and integrate information on injurious mechanical, thermal, and chemical stimuli. Chemical signals either activate nociceptors or modulate their responses to other stimuli. One chemical known to activate or modulate responses of nociceptors is acetylcholine (ACh). Across evolution nociceptors express subunits of the nicotinic acetylcholine receptor (nAChR) family, a family of ACh-gated ion channels. The roles of ACh and nAChRs in nociceptor function are, however, poorly understood. Caenorhabditis elegans polymodal nociceptors, PVD, express nAChR subunits on their sensory arbor. Here we show that mutations reducing ACh synthesis and mutations in nAChR subunits lead to defects in PVD function and morphology. A likely cause for these defects is a reduction in cytosolic calcium measured in ACh and nAChR mutants. Indeed, overexpression of a calcium pump in PVD mimics defects in PVD function and morphology found in nAChR mutants. Our results demonstrate, for the first time, a central role for nAChRs and ACh in nociceptor function and suggest that calcium permeating via nAChRs facilitates activity of several signaling pathways within this neuron.
Indexed as
Identifiers
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.