ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Ocular Dominance Plasticity in Binocular Primary Visual Cortex Does Not Require C1q.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Modeling neurodegeneration in the retina and strategies for developing pan-neurodegenerative therapies.Molecular neurodegeneration · 2025Review
- Experience-dependent control of synaptic remodeling and structural plasticity by glia.Current opinion in neurobiology · 2025Review
- The Influence of Changes in Microglia Development on the Plasticity of the Developing Visual Cortex Circuit in Juvenile Mice.Investigative ophthalmology & visual science · 2025Article
- Article
- Activity-Dependent Synapse Refinement: From Mechanisms to Molecules.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Glia control experience-dependent plasticity in an olfactory critical period.bioRxiv : the preprint server for biology · 2024Article
- Microglia are dispensable for experience-dependent refinement of mouse visual circuitry.Nature neuroscience · 2024Article
- Microglia: Activity-dependent regulators of neural circuits.Annals of the New York Academy of Sciences · 2024Review
- Loss of C1q alters the auditory brainstem response.Frontiers in cellular neuroscience · 2024Article
- Microglia complement signaling promotes neuronal elimination and normal brain functional connectivity.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Review
- The molecular signals that regulate activity-dependent synapse refinement in the brain.Current opinion in neurobiology · 2023Review
- Article
- A Function of Amyloid-β in Mediating Activity-Dependent Axon/Synapse Competition May Unify Its Roles in Brain Physiology and Pathology.Journal of Alzheimer's disease : JAD · 2023Review
- Juvenile depletion of microglia reduces orientation but not high spatial frequency selectivity in mouse V1.Scientific reports · 2022Article
- Synapse-specific plasticity relies on neuroimmune interactions.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Complement and microglia dependent synapse elimination in brain development.WIREs mechanisms of disease · 2022Review
- Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS.Nature reviews. Neuroscience · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
C1q, the initiator of the classical complement cascade, mediates synapse elimination in the postnatal mouse dorsolateral geniculate nucleus of the thalamus and sensorimotor cortex. Here, we asked whether C1q plays a role in experience-dependent synaptic refinement in the visual system at later stages of development. The binocular zone of primary visual cortex (V1b) undergoes spine loss and changes in neuronal responsiveness following the closure of one eye during a defined critical period [a process referred to as ocular dominance plasticity (ODP)]. We therefore hypothesized that ODP would be impaired in the absence of C1q, and that V1b development would also be abnormal without C1q-mediated synapse elimination. However, when we examined several features of V1b development in mice lacking C1q, we found that the densities of most spine populations on basal and proximal apical dendrites, as well as firing rates and ocular dominance, were normal. C1q was only transiently required for the development of spines on apical, but not basal, secondary dendrites. Dendritic morphologies were also unaffected. Although we did not observe the previously described spine loss during ODP in either genotype, our results reveal that the animals lacking C1q had normal shifts in neuronal responsiveness following eye closure. Experiments were performed in both male and female mice. These results suggest that the development and plasticity of the mouse V1b is grossly normal in the absence of C1q.
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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.