ArticleNature communications2022
Selective plasticity of callosal neurons in the adult contralesional cortex following murine traumatic brain injury.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Electroacupuncture Prevents TBI-Induced Synaptic Loss by Inhibiting CaMKII/Drp1-Dependent Mitochondrial Fission.Biomolecules · 2026Article
- Ischemic stroke triggers brain-wide synaptic remodeling within four hours.PLoS biology · 2026Article
- Nrg1 regulates cortical wiring and motor recovery upon traumatic injury.Frontiers in cellular neuroscience · 2026Article
- Cognitive impairment after cerebral ischemia-reperfusion injury: a neuroecosystem perspective.Frontiers in neurology · 2026Review
- Contralateral Structure and Molecular Response to Severe Unilateral Brain Injury.Brain sciences · 2025Article
- Ultrasound-activated piezoelectric nanostickers for neural stem cell therapy of traumatic brain injury.Nature materials · 2025Article
- Extracellular piezoelectric nanostickers promote neuronal differentiation.Nature materials · 2025Article
- Repetitive concussions promote microglia-mediated engulfment of presynaptic excitatory input associated with cognitive dysfunction.Communications biology · 2025Article
- Maintaining Drosha expression with Cdk5 inhibitors as a potential therapeutic strategy for early intervention after TBI.Experimental & molecular medicine · 2024Article
- Plasticity of callosal neurons in the contralesional cortex following traumatic brain injury.Neural regeneration research · 2023Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) results in deficits that are often followed by recovery. The contralesional cortex can contribute to this process but how distinct contralesional neurons and circuits respond to injury remains to be determined. To unravel adaptations in the contralesional cortex, we used chronic in vivo two-photon imaging. We observed a general decrease in spine density with concomitant changes in spine dynamics over time. With retrograde co-labeling techniques, we showed that callosal neurons are uniquely affected by and responsive to TBI. To elucidate circuit connectivity, we used monosynaptic rabies tracing, clearing techniques and histology. We demonstrate that contralesional callosal neurons adapt their input circuitry by strengthening ipsilateral connections from pre-connected areas. Finally, functional in vivo two-photon imaging demonstrates that the restoration of pre-synaptic circuitry parallels the restoration of callosal activity patterns. Taken together our study thus delineates how callosal neurons structurally and functionally adapt following a contralateral murine TBI.
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