ArticleProceedings of the National Academy of Sciences of the United States of America2010
NMDA receptor-dependent GABAB receptor internalization via CaMKII phosphorylation of serine 867 in GABAB1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 109 citations in OpenAlex.
- NAcLat-DBS reduces GABANeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- TAAR1 deficiency impairs mitochondrial dynamics and synaptic integrity in the medial prefrontal cortex and associated cognition in mice.Translational psychiatry · 2025Article
- GABAMedComm · 2025Review
- The E3 ubiquitin ligase MARCH1 mediates downregulation of plasma membrane GABAScientific reports · 2025Article
- Pharmacological mechanism and clinical application of ciprofol.Frontiers in pharmacology · 2025Review
- Optimization of neuron-specific interfering peptides targeting GABAFrontiers in pharmacology · 2025Article
- Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice.Science signaling · 2024Article
- Action of GABAThe journal of physiological sciences : JPS · 2024Article
- Restoring GABAFrontiers in molecular neuroscience · 2024Article
- ERK1/2-Dependent Phosphorylation of GABAInternational journal of molecular sciences · 2023Article
- Ethanol blocks a novel form of iLTD, but not iLTP of inhibitory inputs to VTA GABA neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- The CaMKII-dependent phosphorylation of GABACNS neuroscience & therapeutics · 2023Article
- Targeting the interaction of GABABrain pathology (Zurich, Switzerland) · 2023Article
- The role of GABAFrontiers in endocrinology · 2023Review
- CaMKIIα as a Promising Drug Target for Ischemic Grey Matter.Brain sciences · 2022Review
- CaInternational journal of molecular sciences · 2022Review
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- Protein phosphatase 2A regulation of GABAFrontiers in molecular neuroscience · 2022Article
- Targeting the Interaction of GABAFrontiers in pharmacology · 2022Article
- GABACurrent topics in behavioral neurosciences · 2022Review
11 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GABAB receptors are the G-protein-coupled receptors for GABA, the main inhibitory neurotransmitter in the brain. GABAB receptors are abundant on dendritic spines, where they dampen postsynaptic excitability and inhibit Ca2+ influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals. Here, we show that an excitatory signaling cascade enables spines to counteract this GABAB-mediated inhibition. We found that NMDA application to cultured hippocampal neurons promotes dynamin-dependent endocytosis of GABAB receptors. NMDA-dependent internalization of GABAB receptors requires activation of Ca2+/Calmodulin-dependent protein kinase II (CaMKII), which associates with GABAB receptors in vivo and phosphorylates serine 867 (S867) in the intracellular C terminus of the GABAB1 subunit. Blockade of either CaMKII or phosphorylation of S867 renders GABAB receptors refractory to NMDA-mediated internalization. Time-lapse two-photon imaging of organotypic hippocampal slices reveals that activation of NMDA receptors removes GABAB receptors within minutes from the surface of dendritic spines and shafts. NMDA-dependent S867 phosphorylation and internalization is predominantly detectable with the GABAB1b subunit isoform, which is the isoform that clusters with inhibitory effector K+ channels in the spines. Consistent with this, NMDA receptor activation in neurons impairs the ability of GABAB receptors to activate K+ channels. Thus, our data support that NMDA receptor activity endocytoses postsynaptic GABAB receptors through CaMKII-mediated phosphorylation of S867. This provides a means to spare NMDA receptors at individual glutamatergic synapses from reciprocal inhibition through GABAB receptors.
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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.