ArticleCell reports2016
Phospho-dependent Accumulation of GABABRs at Presynaptic Terminals after NMDAR Activation.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 22 citations in OpenAlex.
- NAcLat-DBS reduces GABANeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Synaptic and intrinsic membrane defects disrupt early neural network dynamics in Down syndrome.Nature communications · 2026Article
- Presynaptic hyperexcitability reversed by positive allosteric modulation of a GABABR epilepsy variant.Brain : a journal of neurology · 2025Article
- Function of the GABAergic System in Diabetic Encephalopathy.Cellular and molecular neurobiology · 2023Review
- CaInternational journal of molecular sciences · 2022Review
- Synapse Formation and Function Across Species: Ancient Roles for CCP, CUB, and TSP-1 Structural Domains.Frontiers in neuroscience · 2022Review
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- Advanced imaging and labelling methods to decipher brain cell organization and function.Nature reviews. Neuroscience · 2021Review
- Molecular mechanism of secreted amyloid-β precursor protein in binding and modulating GABAChemical science · 2021Article
- The organizing principle of GABABasic & clinical pharmacology & toxicology · 2020Review
- Complex formation of APP with GABANature communications · 2019Article
- α-Neurexins Together with α2δ-1 Auxiliary Subunits Regulate CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Wnt Signaling Mediates LTP-Dependent Spine Plasticity and AMPAR Localization through Frizzled-7 Receptors.Cell reports · 2018Article
- Deficits in the activity of presynaptic γ-aminobutyric acid type B receptors contribute to altered neuronal excitability in fragile X syndrome.The Journal of biological chemistry · 2017Article
- Organization and functions of mGlu and GABANature · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Here, we uncover a mechanism for regulating the number of active presynaptic GABAB receptors (GABABRs) at nerve terminals, an important determinant of neurotransmitter release. We find that GABABRs gain access to axon terminals by lateral diffusion in the membrane. Their relative accumulation is dependent upon agonist activation and the presence of the two distinct sushi domains that are found only in alternatively spliced GABABR1a subunits. Following brief activation of NMDA receptors (NMDARs) using glutamate, GABABR diffusion is reduced, causing accumulation at presynaptic terminals in a Ca(2+)-dependent manner that involves phosphorylation of GABABR2 subunits at Ser783. This signaling cascade indicates how synaptically released glutamate can initiate, via a feedback mechanism, increased levels of presynaptic GABABRs that limit further glutamate release and excitotoxicity.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.