ArticleBMC biology2023
Sensing and avoiding sick conspecifics requires Gαi2
Article in BMC biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Loss of the endoplasmic reticulum protein canopy 1 disrupts the function and circuit organization of V2R-expressing vomeronasal sensory neurons.Development (Cambridge, England) · 2026Article
- The Anterior Cingulate Cortex and Prosocial Behavior toward Others in Negative State.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Kirrel3 homophilic adhesion function is required for male-directed aggression and vomeronasal acuity to urine chemosignals.Frontiers in cellular neuroscience · 2026Article
- Calcium Imaging in Olfaction: Non-rodent Mammalian Species.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Type 2 vomeronasal receptor-A4 subfamily: Potential predator sensors in mice.Genesis (New York, N.Y. : 2000) · 2024Review
- Neurobiology of Pathogen Avoidance and Mate Choice: Current and Future Directions.Animals : an open access journal from MDPI · 2024Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRodents utilize chemical cues to recognize and avoid other conspecifics infected with pathogens. Infection with pathogens and acute inflammation alter the repertoire and signature of olfactory stimuli emitted by a sick individual. These cues are recognized by healthy conspecifics via the vomeronasal or accessory olfactory system, triggering an innate form of avoidance behavior. However, the molecular identity of the sensory neurons and the higher neural circuits involved in the detection of sick conspecifics remain poorly understood.
resultsWe employed mice that are in an acute state of inflammation induced by systemic administration of lipopolysaccharide (LPS). Through conditional knockout of the G-protein Gαi2 and deletion of other key sensory transduction molecules (Trpc2 and a cluster of 16 vomeronasal type 1 receptors), in combination with behavioral testing, subcellular Ca
conclusionsOur physiological and behavioral analyses indicate that the sensing and avoidance of LPS-treated sick conspecifics depend on the Gαi2 vomeronasal subsystem. Our observations point to a central role of brain circuits downstream of the olfactory periphery and in the lateral habenula in the detection and avoidance of sick conspecifics, providing new insights into the neural substrates and circuit logic of the sensing of inflammation in mice.
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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.