ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Snapin is critical for presynaptic homeostatic plasticity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
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- Whole Genome Sequencing Revealed Inherited Rare Oligogenic Variants Contributing to Schizophrenia and Major Depressive Disorder in Two Families.International journal of molecular sciences · 2023Article
- Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.Frontiers in cellular neuroscience · 2023Article
- Precise mapping of one classic and three novelmicroPublication biology · 2023Article
- The E3 ligase Thin controls homeostatic plasticity through neurotransmitter release repression.eLife · 2022Article
- Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021Article
- Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150Molecular brain · 2021Article
- SNAPIN Regulates Cell Cycle Progression to Promote Pancreatic β Cell Growth.Frontiers in endocrinology · 2021Article
- Neto-α Controls Synapse Organization and Homeostasis at the Drosophila Neuromuscular Junction.Cell reports · 2020Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
- Cul3 and insomniac are required for rapid ubiquitination of postsynaptic targets and retrograde homeostatic signaling.Nature communications · 2019Article
- Maintenance of homeostatic plasticity at theeLife · 2019Article
- Synapse-specific and compartmentalized expression of presynaptic homeostatic potentiation.eLife · 2018Article
- Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.Developmental neurobiology · 2018Review
- Overexpression of cypin alters dendrite morphology, single neuron activity, and network properties via distinct mechanisms.Journal of neural engineering · 2018Article
- Dysbindin links presynaptic proteasome function to homeostatic recruitment of low release probability vesicles.Nature communications · 2018Article
- Sleep/Wake Disruption in a Mouse Model of BLOC-1 Deficiency.Frontiers in neuroscience · 2018Article
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus.Frontiers in genetics · 2017Article
- The Proteome of BLOC-1 Genetic Defects Identifies the Arp2/3 Actin Polymerization Complex to Function Downstream of the Schizophrenia Susceptibility Factor Dysbindin at the Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms underlying the homeostatic modulation of presynaptic neurotransmitter release are largely unknown. We have previously used an electrophysiology-based forward genetic screen to assess the function of >400 neuronally expressed genes for a role in the homeostatic control of synaptic transmission at the neuromuscular junction of Drosophila melanogaster. This screen identified a critical function for dysbindin, a gene linked to schizophrenia in humans (Dickman and Davis, 2009). Biochemical studies in other systems have shown that Snapin interacts with Dysbindin, prompting us to test whether Snapin might be involved in the mechanisms of synaptic homeostasis. Here, we demonstrate that loss of snapin blocks the homeostatic modulation of presynaptic vesicle release following inhibition of postsynaptic glutamate receptors. This is true for both the rapid induction of synaptic homeostasis induced by pharmacological inhibition of postsynaptic glutamate receptors, and the long-term expression of synaptic homeostasis induced by the genetic deletion of the muscle-specific GluRIIA glutamate receptor subunit. Loss of snapin does not alter baseline synaptic transmission, synapse morphology, synapse growth, or the number or density of active zones, indicating that the block of synaptic homeostasis is not a secondary consequence of impaired synapse development. Additional genetic evidence suggests that snapin functions in concert with dysbindin to modulate vesicle release and possibly homeostatic plasticity. Finally, we provide genetic evidence that the interaction of Snapin with SNAP25, a component of the SNARE complex, is also involved in synaptic homeostasis.
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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.