ArticleProceedings of the National Academy of Sciences of the United States of America2010
Prolonged activation of NMDA receptors promotes dephosphorylation and alters postendocytic sorting of GABAB receptors.
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 78 papers.
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Who cites it
78 citing papers in PubMed, 123 citations in OpenAlex.
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- State of the art: glioma-associated epilepsy-bridging tumor biology and epileptogenesis.Neurological research and practice · 2025Review
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- AMPK as a Therapeutic Target: Advancing Epilepsy Management Through Metabolic Modulation.Molecular neurobiology · 2025Review
- The E3 ubiquitin ligase MARCH1 mediates downregulation of plasma membrane GABAScientific reports · 2025Article
- KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.Frontiers in molecular neuroscience · 2025Article
- Optimization of neuron-specific interfering peptides targeting GABAFrontiers in pharmacology · 2025Article
- Restoring GABAFrontiers in molecular neuroscience · 2024Article
- Role of Rab10 in cocaine-induced behavioral effects is associated with GABAB receptor membrane expression in the nucleus accumbens.Frontiers in pharmacology · 2024Article
- Article
- Restoration of GABANeural regeneration research · 2023Article
- 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
- Sigma-1 receptor and seizures.Pharmacological research · 2023Review
- Review
- Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023Review
- Targeting the interaction of GABABrain pathology (Zurich, Switzerland) · 2023Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
Slow and persistent synaptic inhibition is mediated by metabotropic GABAB receptors (GABABRs). GABABRs are responsible for the modulation of neurotransmitter release from presynaptic terminals and for hyperpolarization at postsynaptic sites. Postsynaptic GABABRs are predominantly found on dendritic spines, adjacent to excitatory synapses, but the control of their plasma membrane availability is still controversial. Here, we explore the role of glutamate receptor activation in regulating the function and surface availability of GABABRs in central neurons. We demonstrate that prolonged activation of NMDA receptors (NMDA-Rs) leads to endocytosis, a diversion from a recycling route, and subsequent lysosomal degradation of GABABRs. These sorting events are paralleled by a reduction in GABABR-dependent activation of inwardly rectifying K+ channel currents. Postendocytic sorting is critically dependent on phosphorylation of serine 783 (S783) within the GABABR2 subunit, an established substrate of AMP-dependent protein kinase (AMPK). NMDA-R activation leads to a rapid increase in phosphorylation of S783, followed by a slower dephosphorylation, which results from the activity of AMPK and protein phosphatase 2A, respectively. Agonist activation of GABABRs counters the effects of NMDA. Thus, NMDA-R activation alters the phosphorylation state of S783 and acts as a molecular switch to decrease the abundance of GABABRs at the neuronal plasma membrane. Such a mechanism may be of significance during synaptic plasticity or pathological conditions, such as ischemia or epilepsy, which lead to prolonged activation of glutamate 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.