ArticleNeuron2026
Tachykinin signaling defines distinct populations of glia in the enteric nervous system.
Article in Neuron, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Intestinal muscularis in health and disease.Communications biology · 2026Review
- Neurokinin receptor antagonists for vasomotor symptoms: from KNDy neurons to clinical translation.Nature reviews. Endocrinology · 2026Review
- Enteric Glial Network in Diabetes: Quantitative Changes of Glial Density in Rats in Response to Acute and Chronic Hyperglycaemia.Biomedicines · 2026Article
- Macrophage-glia interactions regulate immune damage to enteric neurons during West Nile virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enteric glial cells as regulators of the gut-brain axis: hormonal signaling, stress responses and progenitor potential.Frontiers in neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
One of the largest glial populations outside the brain is in the gut. These enteric glia are involved in many functions, from intestinal peristalsis to immunity, yet it is unclear whether subtypes exist with distinct roles in homeostasis. Comparing glia from divergent microenvironments in the mouse intestine, we found that mucosal glia most resembled microglia, while muscularis glia resembled satellite glia. Tacr3, encoding the receptor for neuropeptide neurokinin B (NKB), was enriched within muscularis glia associated with neuronal soma and was undetectable in extraintestinal glia. Genetic or pharmacological manipulation of NKB-TACR3 signaling disrupted the establishment of enteric glial populations during postnatal development and dynamically modulated intestinal motor behaviors in adult mice. Collectively, we delineate spatially, transcriptionally, and functionally distinct populations of enteric glia; identify one as an unanticipated target of TACR3 antagonists in clinical use; and establish this pathway as necessary for enteric glial diversification and function.
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Registered trials
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