ArticleNature communications2024
Neuroprotective gap-junction-mediated bystander transformations in the adult zebrafish spinal cord after injury.
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.
- Small extracellular vesicle-integrated by herbal hydrogels for spatiotemporal immunomodulation and neurovascular repair following traumatic brain injury.Bioactive materials · 2026Article
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- Time-dependent adaptations of damaged neurons and their microenvironment in the regenerating adult zebrafish spinal cord.Science advances · 2026Article
- Priming neuronal regeneration: early adaptive mechanisms in zebrafish CNS injury.Frontiers in molecular neuroscience · 2026Review
- Mechanisms underpinning spontaneous spinal cord regeneration.Development (Cambridge, England) · 2025Review
- Blueprints for healing: central nervous system regeneration in zebrafish and neonatal mice.BMC biology · 2025Review
- Modeling traumatic brain and neural injuries: insights from zebrafish.Frontiers in molecular neuroscience · 2025Review
- Endoplasmic reticulum stress-related deficits in calcium clearance promote neuronal dysfunction that is prevented by SERCA2 gene augmentation.Cell reports. Medicine · 2024Article
- Neural Influences on Tumor Progression Within the Central Nervous System.CNS neuroscience & therapeutics · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The adult zebrafish spinal cord displays an impressive innate ability to regenerate after traumatic insults, yet the underlying adaptive cellular mechanisms remain elusive. Here, we show that while the cellular and tissue responses after injury are largely conserved among vertebrates, the large-size fast spinal zebrafish motoneurons are remarkably resilient by remaining viable and functional. We also reveal the dynamic changes in motoneuron glutamatergic input, excitability, and calcium signaling, and we underscore the critical role of calretinin (CR) in binding and buffering the intracellular calcium after injury. Importantly, we demonstrate the presence and the dynamics of a neuron-to-neuron bystander neuroprotective biochemical cooperation mediated through gap junction channels. Our findings support a model in which the intimate and dynamic interplay between glutamate signaling, calcium buffering, gap junction channels, and intercellular cooperation upholds cell survival and promotes the initiation of regeneration.
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Registered trials
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