ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025
CXCL12 Engages Cortical Inhibitory Neurons to Enhance Dendritic Spine Plasticity and Structured Network Activity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Chemokine levels in the murine brain from early postnatal development to aging.Brain, behavior, & immunity - health · 2026Article
- Attract to kill: Exploring the potential of motility trapping as a novel treatment strategy for high-grade gliomas.Neuro-oncology · 2026Review
- Decoding Neuroinflammatory Pathways: The Role of the CXCL12-CXCR4/CXCR7 Axis in ALS-Related Cognitive Impairment.Molecular neurobiology · 2026Review
- CXCL12/CXCR4 axis in neuropathic pain: Insights from preclinical models and translational implications.Molecular painReview
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The chemokine CXCL12 is a highly conserved peptide that regulates homeostatic processes in the brain throughout life. Recent work shows that CXCL12 increases dendritic spine density in cortical neurons, which requires activation of CXCL12's receptor CXCR4. This same pathway reverses cortical dendritic spine deficits and cognitive impairment in an animal model of neuroHIV. However, it remained unclear if CXCL12 simply preserved existing spines or also engaged spine plasticity processes that drove network-level adaptations. We therefore tested if CXCL12 could regulate dendritic spine turnover, maturation, clustering, and neuronal network activity in primary rat cortical neurons of either sex using live-cell imaging, confocal microscopy, and multielectrode arrays. Intriguingly, CXCL12-treated neurons formed significantly more new spines than controls, and this outcome was blocked by the CXCR4 antagonist AMD3100. CXCL12 also increased the density of thin spines expressing postsynaptic markers, including postsynaptic density protein 95 (PSD-95), phospho-PSD-95
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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.