ArticleNature communications2024
Molecular and circuit mechanisms underlying avoidance of rapid cooling stimuli in C. elegans.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Comparative connectomics reveals stage-specific gap junction rewiring that reshapes avoidance behavior.bioRxiv : the preprint server for biology · 2026Article
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- Hungry for Knowledge: Octopamine Signaling Regulates Hunger-Enhanced Olfactory Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Glial Hub-and-Spoke Circuitry in C. elegans orchestrates bidirectional thermosensation.Nature communications · 2026Article
- Understanding animal temperature sensation: from molecular thermosensors to physiological impacts.Science China. Life sciences · 2026Review
- Serotonergic Signaling GovernseNeuro · 2025Article
- TheiScience · 2025Article
- Thermosensory Roles of G Protein-Coupled Receptors and Other Cellular Factors in Animals.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms by which animals respond to rapid changes in temperature are largely unknown. Here, we found that polymodal ASH sensory neurons mediate rapid cooling-evoked avoidance behavior within the physiological temperature range in C. elegans. ASH employs multiple parallel circuits that consist of stimulatory circuits (AIZ, RIA, AVA) and disinhibitory circuits (AIB, RIM) to respond to rapid cooling. In the stimulatory circuit, AIZ, which is activated by ASH, releases glutamate to act on both GLR-3 and GLR-6 receptors in RIA neurons to promote reversal, and ASH also directly or indirectly stimulates AVA to promote reversal. In the disinhibitory circuit, AIB is stimulated by ASH through the GLR-1 receptor, releasing glutamate to act on AVR-14 to suppress RIM activity. RIM, an inter/motor neuron, inhibits rapid cooling-evoked reversal, and the loop activities thus equally stimulate reversal. Our findings elucidate the molecular and circuit mechanisms underlying the acute temperature stimuli-evoked avoidance behavior.
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Registered trials
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