ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Compartmentalization of the GABAB receptor signaling complex is required for presynaptic inhibition at hippocampal synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Developmental regulation of GABAHistology and histopathology · 2025Article
- Synaptotagmin-11 facilitates assembly of a presynaptic signaling complex in post-Golgi cargo vesicles.EMBO reports · 2024Article
- Monoacylglycerol Lipase Protects the Presynaptic Cannabinoid 1 Receptor from Desensitization by Endocannabinoids after Persistent Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- GABAeLife · 2023Article
- The β-cell primary cilium is an autonomous Ca2+ compartment for paracrine GABA signaling.The Journal of cell biology · 2023Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- Visualization of β-adrenergic receptor dynamics and differential localization in cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Neurexins regulate presynaptic GABANature communications · 2021Article
- The life cycle of voltage-gated CaNeuronal signaling · 2021Review
- Cellular Diversity and Differential Subcellular Localization of the G-Protein GFrontiers in neuroanatomy · 2021Article
- Firing rate homeostasis counteracts changes in stability of recurrent neural networks caused by synapse loss in Alzheimer's disease.PLoS computational biology · 2020Article
- Article
- Differential association of GABABrain structure & function · 2018Article
- Muscle afferent excitability testing in spinal root-intact rats: dissociating peripheral afferent and efferent volleys generated by intraspinal microstimulation.Journal of neurophysiology · 2017Article
- Presynaptic GABAB receptors reduce transmission at parabrachial synapses in the lateral central amygdala by inhibiting N-type calcium channels.Scientific reports · 2016Article
- Article
- GABAB receptor deficiency causes failure of neuronal homeostasis in hippocampal networks.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Modulation of synaptic function through the α-neurexin-specific ligand neurexophilin-1.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Complex GABAB receptor complexes: how to generate multiple functionally distinct units from a single receptor.Frontiers in pharmacology · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Presynaptic inhibition via G-protein-coupled receptors (GPCRs) and voltage-gated Ca(2+) channels constitutes a widespread regulatory mechanism of synaptic strength. Yet, the mechanism of intermolecular coupling underlying GPCR-mediated signaling at central synapses remains unresolved. Using FRET spectroscopy, we provide evidence for formation of spatially restricted (<100 Å) complexes between GABA(B) receptors composed of GB(1a)/GB(2) subunits, Gα(o)β(1)γ(2) G-protein heterotrimer, and Ca(V)2.2 channels in hippocampal boutons. GABA release was not required for the assembly but for structural reorganization of the precoupled complex. Unexpectedly, GB(1a) deletion disrupted intermolecular associations within the complex. The GB(1a) proximal C-terminal domain was essential for association of the receptor, Ca(V)2.2 and Gβγ, but was dispensable for agonist-induced receptor activation and cAMP inhibition. Functionally, boutons lacking this complex-formation domain displayed impaired presynaptic inhibition of Ca(2+) transients and synaptic vesicle release. Thus, compartmentalization of the GABA(B1a) receptor, Gβγ, and Ca(V)2.2 channel in a signaling complex is required for presynaptic inhibition at hippocampal synapses.
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What Socratic holds
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 Socratic graph.