ArticleG3 (Bethesda, Md.)2014
Dopamine signaling in C. elegans is mediated in part by HLH-17-dependent regulation of extracellular dopamine levels.
Article in G3 (Bethesda, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 23 citations in OpenAlex.
- Marine bacterium Stutzerimonas stutzeri mitigates Parkinson's disease pathology in C. elegans via ferroptosis modulation.Scientific reports · 2026Article
- The dopaminergic system ofRoyal Society open science · 2025Review
- ZA-II-05, a novel NMDA-receptor antagonist reverses vanadium-induced neurotoxicity in Caenorhabditis elegans (C. elegans).BMC neuroscience · 2024Article
- Amphetamine exposure during embryogenesis changes expression and function of the dopamine transporter in Caenorhabditis elegans offspring.Journal of neurochemistry · 2024Article
- Dopaminergic modulation by quercetin: In silico and in vivo evidence using Caenorhabditis elegans as a model.Chemico-biological interactions · 2023Article
- Article
- A novel de novo FEM1C variant is linked to neurodevelopmental disorder with absent speech, pyramidal signs and limb ataxia.Human molecular genetics · 2023Article
- The dopamine membrane transporter plays an active modulatory role in synaptic dopamine homeostasis.Journal of neuroscience research · 2022Article
- Translational relevance of forward genetic screens in animal models for the study of psychiatric disease.Neuroscience and biobehavioral reviews · 2022Review
- Inferences of glia-mediated control in Caenorhabditis elegans.Journal of neuroscience research · 2021Article
- Evolutionary Origins of the Oligodendrocyte Cell Type and Adaptive Myelination.Frontiers in neuroscience · 2021Review
- Swimming Induced Paralysis to Assess Dopamine Signaling in Caenorhabditis elegans.Journal of visualized experiments : JoVE · 2019Article
- Lead (Pb) exposure induces dopaminergic neurotoxicity inToxicology reports · 2019Article
- From the Cover: Harmane-Induced Selective Dopaminergic Neurotoxicity in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- The Neuroendocrine-Immune Regulation in Response to Environmental Stress in Marine Bivalves.Frontiers in physiology · 2018Review
- Glial Expression of the Caenorhabditis elegans Gene swip-10 Supports Glutamate Dependent Control of Extrasynaptic Dopamine Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
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2 authors at 1 institution in 1 country.
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Abstract
In Caenorhabditis elegans, the dopamine transporter DAT-1 regulates synaptic dopamine (DA) signaling by controlling extracellular DA levels. In dat-1(ok157) animals, DA is not taken back up presynaptically but instead reaches extrasynpatic sites, where it activates the dopamine receptor DOP-3 on choligeneric motor neurons and causes animals to become paralyzed in water. This phenotype is called swimming-induced paralysis (SWIP) and is dependent on dat-1 and dop-3. Upstream regulators of dat-1 and dop-3 have yet to be described in C. elegans. In our previous studies, we defined a role for HLH-17 during dopamine response through its regulation of the dopamine receptors. Here we continue our characterization of the effects of HLH-17 on dopamine signaling. Our results suggest that HLH-17 acts downstream of dopamine synthesis to regulate the expression of dop-3 and dat-1. First, we show that hlh-17 animals display a SWIP phenotype that is consistent with its regulation of dop-3 and dat-1. Second, we show that this behavior is enhanced by treatment with the dopamine reuptake inhibitor, bupropion, in both hlh-17 and dat-1 animals, a result suggesting that SWIP behavior is regulated via a mechanism that is both dependent on and independent of DAT-1. Third, and finally, we show that although the SWIP phenotype of hlh-17 animals is unresponsive to the dopamine agonist, reserpine, and to the antidepressant, fluoxetine, hlh-17 animals are not defective in acetylcholine signaling. Taken together, our work suggests that HLH-17 is required to maintain normal levels of dopamine in the synaptic cleft through its regulation of dop-3 and dat-1.
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