ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Long-term nicotine adaptation in Caenorhabditis elegans involves PKC-dependent changes in nicotinic receptor abundance.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 80 citations in OpenAlex.
- Nicotine induces abnormal motor coupling through sensitization of a mechanosensory circuit in Caenorhabditis elegans.PLoS biology · 2025Article
- Nicotine Motivated Behavior inInternational journal of molecular sciences · 2024Article
- Semantic Representation of Neural Circuit Knowledge inbioRxiv : the preprint server for biology · 2023Article
- Calcineurin-Dependent Homeostatic Response ofCells · 2023Article
- Modelling organophosphate intoxication in C. elegans highlights nicotinic acetylcholine receptor determinants that mitigate poisoning.PloS one · 2023Article
- Bi-allelic loss-of-function variants in PPFIBP1 cause a neurodevelopmental disorder with microcephaly, epilepsy, and periventricular calcifications.American journal of human genetics · 2022Article
- Article
- Cellular Expression and Functional Roles of All 26 Neurotransmitter GPCRs in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Investigation of feeding behaviour in C. elegans reveals distinct pharmacological and antibacterial effects of nicotine.Invertebrate neuroscience : IN · 2018Article
- Short-term nicotine exposure induces long-lasting modulation of gustatory plasticity inBiochemistry and biophysics reports · 2016Article
- Activity of theeLife · 2016Article
- Caenorhabditis elegans as a Model to Study the Molecular and Genetic Mechanisms of Drug Addiction.Progress in molecular biology and translational science · 2016Review
- Drug-dependent behaviors and nicotinic acetylcholine receptor expressions in Caenorhabditis elegans following chronic nicotine exposure.Neurotoxicology · 2015Article
- Nematodes feel a craving--using Caenorhabditis elegans as a model to study alcohol addiction.Neuroscience bulletin · 2014Review
- Chronic nicotine exposure systemically alters microRNA expression profiles during post-embryonic stages in Caenorhabditis elegans.Journal of cellular physiology · 2014Article
- Impacts of chronic low-level nicotine exposure on Caenorhabditis elegans reproduction: identification of novel gene targets.Reproductive toxicology (Elmsford, N.Y.) · 2013Article
- Postsynaptic ERG potassium channels limit muscle excitability to allow distinct egg-laying behavior states in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- PKC-2 phosphorylation of UNC-18 Ser322 in AFD neurons regulates temperature dependency of locomotion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Role of protein kinase C β and vascular endothelial growth factor receptor in malignant pleural mesothelioma: Therapeutic implications and the usefulness of Caenorhabditis elegans model organism.Journal of carcinogenesis · 2011Article
- Therapeutic opportunities of small interfering RNA.Fundamental & clinical pharmacology · 2009Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic exposure to nicotine leads to long-term changes in both the abundance and activity of nicotinic acetylcholine receptors, processes thought to contribute to nicotine addiction. We have found that in Caenorhabditis elegans, prolonged nicotine treatment results in a long-lasting decrease in the abundance of nicotinic receptors that control egg-laying. In naive animals, acute exposure to cholinergic agonists led to the efficient stimulation of egg-laying, a response mediated by a nicotinic receptor functionally expressed in the vulval muscle cells. Overnight exposure to nicotine led to a specific and long-lasting change in egg-laying behavior, which rendered the nicotine-adapted animals insensitive to simulation of egg-laying by the nicotinic agonist and was accompanied by a promoter-independent reduction in receptor protein levels. Mutants defective in the gene tpa-1, which encodes a homolog of protein kinase C (PKC), failed to undergo adaptation to nicotine; after chronic nicotine exposure they remained sensitive to cholinergic agonists and retained high levels of receptor protein in the vulval muscles. These results suggest that PKC-dependent signaling pathways may promote nicotine adaptation via regulation of nicotinic receptor synthesis or degradation.
Indexed as
Identifiers
11102488PMC6773091W2167458669What 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.