ArticleNature communications2024
Selective vulnerability of parvocellular oxytocin neurons in social dysfunction.
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.
What it found
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Who cites it
9 citing papers in PubMed.
- Transcriptomic landscape of microglia in mouse models of social dysfunction and oxytocin-mediated recovery.iScience · 2026Article
- Mapping of oxytocin- and arginine vasopressin-expressing neurons with calbindin 1 or reelin in the male mouse brain.Journal of neuroendocrinology · 2026Article
- Conditional deletion of Cc2d1a increases irritability-like behavior by decreasing oxytocin expression via the prelimbic-hypothalamic pathway.Journal of biomedical science · 2026Article
- Prostaglandin signaling drives peripheral inflammation-induced reduction of hypothalamic oxytocin-positive neurons.Cellular and molecular life sciences : CMLS · 2026Article
- Astrocytes mediate a positive feedback loop for oxytocin.bioRxiv : the preprint server for biology · 2026Article
- Three-dimensional quantification of oxytocin neurons in the hypothalamic paraventricular nucleus reveals sex- and subregion-specific differences in two genetic mouse models of autism.Journal of neuroendocrinology · 2025Article
- Cocaine-context memories are transcriptionally encoded in nucleus accumbens Arc ensembles.Nature communications · 2025Article
- Navigating Central Oxytocin Transport: Known Realms and Uncharted Territories.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Flexible adjustment of oxytocin neuron activity in mouse dams revealed by microendoscopy.Science advances · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Selective vulnerability offers a conceptual framework for understanding neurodegenerative disorders such as Parkinson's disease, where specific neuronal types are selectively affected and adjacent ones are spared. However, the applicability of this framework to neurodevelopmental disorders, particularly those characterized by atypical social behaviors, such as autism spectrum disorder, remains uncertain. Here we show that an embryonic disturbance, known to induce social dysfunction in male mice, preferentially impaired the gene expression crucial for neural functions in parvocellular oxytocin (OT) neurons-a subtype linked to social rewards-while neighboring cell types experienced a lesser impact. Chemogenetic stimulation of OT neurons at the neonatal stage ameliorated social deficits in early adulthood, concurrent with cell-type-specific sustained recovery of pivotal gene expression within parvocellular OT neurons. Collectively, our data shed light on the transcriptomic selective vulnerability within the hypothalamic social behavioral center and provide a potential therapeutic target through specific neonatal neurostimulation.
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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.