ArticleeLife2016
Astrocytes contribute to synapse elimination via type 2 inositol 1,4,5-trisphosphate receptor-dependent release of ATP.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 86 citations in OpenAlex.
- The role of zinc homeostasis in major depressive disorder: heterogeneous pathological mechanisms and therapeutic implications.Annals of medicine · 2026Review
- Oral Recombinant Human Collagen III Protects Gastric Mucosa via G-Quadruplex-Mediated Activation of the Pla2g4a-Prostaglandin Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of astrocytes in autism spectrum disorder and associated syndromes: Evidence, animal models, mechanisms, and therapeutic potential.Zoological research · 2026Review
- The glia-immune network: Astrocytes and oligodendrocytes as microglial co-ordinators in health and disease.The Journal of physiology · 2026Review
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Potential roles for microglia in drug addiction: Adolescent neurodevelopment and beyond.Journal of neuroimmunology · 2025Review
- The Role of Astrocytes in the Molecular Pathophysiology of Schizophrenia: Between Neurodevelopment and Neurodegeneration.Biomolecules · 2025Review
- Developmental Impairments of Synaptic Refinement in the Thalamus of a Mouse Model of Fragile X Syndrome.Neuroscience bulletin · 2024Article
- Major depressive disorder: hypothesis, mechanism, prevention and treatment.Signal transduction and targeted therapy · 2024Review
- The neurobiological mechanisms and therapeutic prospect of extracellular ATP in depression.CNS neuroscience & therapeutics · 2024Review
- Astrocytes Excessively Engulf Synapses in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Review
- Mitochondrial fission drives neuronal metabolic burden to promote stress susceptibility in male mice.Nature metabolism · 2023Article
- Intercellular contact and cargo transfer between Müller glia and to microglia precede apoptotic cell clearance in the developing retina.bioRxiv : the preprint server for biology · 2023Article
- Bridging a mechanistic gap from diet to synapses.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neurexin and neuroligins jointly regulate synaptic degeneration at theFrontiers in cellular neuroscience · 2023Article
- A short period of early life oxytocin treatment rescues social behavior dysfunction via suppression of hippocampal hyperactivity in male mice.Molecular psychiatry · 2022Article
- Connexin 43: insights into candidate pathological mechanisms of depression and its implications in antidepressant therapy.Acta pharmacologica Sinica · 2022Review
- A distinct astrocyte subtype in the aging mouse brain characterized by impaired protein homeostasis.Nature aging · 2022Article
- Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Selective elimination of unwanted synapses is vital for the precise formation of neuronal circuits during development, but the underlying mechanisms remain unclear. Using inositol 1,4,5-trisphosphate receptor type 2 knockout (Itpr2(-/-)) mice to specifically disturb somatic Ca(2+) signaling in astrocytes, we showed that developmental elimination of the ventral posteromedial nucleus relay synapse was impaired. Interestingly, intracerebroventricular injection of ATP, but not adenosine, rescued the deficit in synapse elimination in Itpr2(-/-) mice. Further studies showed that developmental synapse elimination was also impaired in P2ry1(-/-) mice and was not rescued by ATP, indicating a possible role of purinergic signaling. This hypothesis was confirmed by MRS-2365, a selective P2Y1 agonist, could also rescue the deficient of synapse elimination in Itpr2(-/-) mice. Our results uncovered a novel mechanism suggesting that astrocytes release ATP in an IP3R2-dependent manner to regulate synapse elimination.
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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.