ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
SPARCL1 Promotes Excitatory But Not Inhibitory Synapse Formation and Function Independent of Neurexins and Neuroligins.
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 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Deciphering cell-type-and temporally specific matrisome expression signatures in human cortical development and neurodevelopmental disorders via scRNA-seq meta-analysis.Nature communications · 2025Pooled it
- Teneurins Are SPARCL1 Receptors.bioRxiv : the preprint server for biology · 2026Article
- Hevin/sparcl-1 as a potential biomarker and therapy in age-associated cognitive decline.Neural regeneration research · 2026Article
- SPARCL1 Enrichment at the Glioblastoma Invasive Front Is Consistent with Synaptogenic and Angiogenic Tumor Niches.International journal of molecular sciences · 2026Article
- Elovanoid neuroprotection targets cell transcriptomics and proteomics to sustain synaptic integrity after brain injury.Communications biology · 2026Article
- Weaker neuroligin 2-neurexin β1 interaction tethers membranes and recruits gephyrin at membrane junctions through clustering.Science advances · 2026Article
- Altered tear fluid protein expression in persons with mild cognitive impairment.Journal of Alzheimer's disease : JAD · 2026Article
- Chimeric brain models to study human glial-neuronal and macroglial-microglial interactions.Cell reports · 2026Article
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Progressive changes in synapses and glial cells inBrain communications · 2026Article
- Astrocytes Control Cocaine-Induced Synaptic Plasticity and Reward Through the Matricellular Protein Hevin.Biological psychiatry · 2025Article
- Glioma-derived SPARCL1 promotes the formation of peritumoral neuron-glioma synapses.Journal of neuro-oncology · 2025Article
- Neuroinflammation Markers in Tear Fluid of Mild Alzheimer's Disease.Journal of molecular neuroscience : MN · 2025Article
- Astrocytic Hevin/SPARCL-1 Regulates Cognitive Decline in Pathological and Normal Brain Aging.Aging cell · 2025Article
- The lung microvasculature promotes alveolar type 2 cell differentiation via secreted SPARCL1.Stem cell reports · 2025Article
- Identification of candidate genes involved in Zika virus-induced reversible paralysis of mice.Scientific reports · 2025Article
- Perturbed synaptic adhesion molecules signaling in neurodevelopmental disorders: The impact of metal neurotoxicity.Ibrain · 2025Review
- Radio-chemotherapy and metformin selectively modulate the heterogeneous landscape of glioma with ribosome biogenesis, long non coding RNA and immune-escape markers as major player.International journal of biological sciences · 2025Article
- Chronic stress induces depression through MDGA1-Neuroligin2 mediated suppression of inhibitory synapses in the lateral habenula.Theranostics · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Emerging evidence supports roles for secreted extracellular matrix proteins in boosting synaptogenesis, synaptic transmission, and synaptic plasticity. SPARCL1 (also known as Hevin), a secreted non-neuronal protein, was reported to increase synaptogenesis by simultaneously binding to presynaptic neurexin-1α and to postsynaptic neuroligin-1B, thereby catalyzing formation of trans-synaptic neurexin/neuroligin complexes. However, neurexins and neuroligins do not themselves mediate synaptogenesis, raising the question of how SPARCL1 enhances synapse formation by binding to these molecules. Moreover, it remained unclear whether SPARCL1 acts on all synapses containing neurexins and neuroligins or only on a subset of synapses, and whether it enhances synaptic transmission in addition to boosting synaptogenesis or induces silent synapses. To explore these questions, we examined the synaptic effects of SPARCL1 and their dependence on neurexins and neuroligins. Using mixed neuronal and glial cultures from neonatal mouse cortex of both sexes, we show that SPARCL1 selectively increases excitatory but not inhibitory synapse numbers, enhances excitatory but not inhibitory synaptic transmission, and augments NMDAR-mediated synaptic responses more than AMPAR-mediated synaptic responses. None of these effects were mediated by SPARCL1-binding to neurexins or neuroligins. Neurons from triple
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