ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Phospholipase C is required for changes in postsynaptic structure and function associated with NMDA receptor-dependent long-term depression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 104 citations in OpenAlex.
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Phospholipase C beta 1 in the dentate gyrus gates fear memory formation through regulation of neuronal excitability.Science advances · 2024Article
- MARCKS and PI(4,5)PMolecular biology of the cell · 2024Article
- Proteomic association with age-dependent sex differences in Wisconsin Card Sorting Test performance in healthy Thai subjects.Scientific reports · 2023Article
- Long-term depression in neurons involves temporal and ultra-structural dynamics of phosphatidylinositol-4,5-bisphosphate relying on PIP5K, PTEN and PLC.Communications biology · 2023Article
- Vir2Drug: a drug repurposing framework based on protein similarities between pathogens.Briefings in bioinformatics · 2023Article
- Signaling pathways involved in NMDA-induced suppression of M-channels in corticotropin-releasing hormone neurons in central amygdala.Journal of neurochemistry · 2022Article
- Hippocampal neurons maintain a large PtdIns(4)P pool that results in faster PtdIns(4,5)P2 synthesis.The Journal of general physiology · 2022Article
- A computational model of dopaminergic modulation of hippocampal Schaffer collateral-CA1 long-term plasticity.Journal of computational neuroscience · 2022Article
- Palmitoylation of A-kinase anchoring protein 79/150 modulates its nanoscale organization, trafficking, and mobility in postsynaptic spines.Frontiers in synaptic neuroscience · 2022Article
- Editorial: The key role of lipids in the regulation of ion channels.Frontiers in physiology · 2022Article
- Spotlight on the Binding Affinity of Ion Channels for Phosphoinositides: From the Study of Sperm Flagellum.Frontiers in physiology · 2022Review
- Nanoscale Sub-Compartmentalization of the Dendritic Spine Compartment.Biomolecules · 2021Review
- Phosphorylation-Dependent Regulation of CaFrontiers in synaptic neuroscience · 2020Article
- The epilepsy and intellectual disability-associated protein TBC1D24 regulates the maintenance of excitatory synapses and animal behaviors.PLoS genetics · 2020Article
- Early Downregulation of p75Molecular neurobiology · 2019Article
- Functional and Structural Impairments in the Perirhinal Cortex of a Mouse Model of CDKL5 Deficiency Disorder Are Rescued by a TrkB Agonist.Frontiers in cellular neuroscience · 2019Article
- Metabotropic Acetylcholine and Glutamate Receptors Mediate PI(4,5)PScientific reports · 2018Article
- Glutamatergic Signaling in the Central Nervous System: Ionotropic and Metabotropic Receptors in Concert.Neuron · 2018Review
- Potential for therapeutic targeting of AKAP signaling complexes in nervous system disorders.Pharmacology & therapeutics · 2018Review
7 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
NMDA receptor (NMDAR)-dependent hippocampal synaptic plasticity underlying learning and memory coordinately regulates dendritic spine structure and AMPA receptor (AMPAR) postsynaptic strength through poorly understood mechanisms. Induction of long-term depression (LTD) activates protein phosphatase 2B/calcineurin (CaN), leading to dendritic spine shrinkage through actin depolymerization and AMPAR depression through receptor dephosphorylation and internalization. The scaffold proteins A-kinase-anchoring protein 79/150 (AKAP79/150) and postsynaptic density 95 (PSD95) form a complex that controls the opposing actions of the cAMP-dependent protein kinase (PKA) and CaN in regulation of AMPAR phosphorylation. The AKAP79/150-PSD95 complex is disrupted in hippocampal neurons during LTD coincident with internalization of AMPARs, decreases in PSD95 levels, and loss of AKAP79/150 and PKA from spines. AKAP79/150 is targeted to spines through binding F-actin and the phospholipid phosphatidylinositol-(4,5)-bisphosphate (PIP2). Previous electrophysiological studies have demonstrated that inhibition of phospholipase C (PLC)-catalyzed hydrolysis of PIP2 inhibits NMDAR-dependent LTD; however, the signaling mechanisms that link PLC activation to alterations in dendritic spine structure and AMPAR function in LTD are unknown. We show here that NMDAR stimulation of PLC in cultured hippocampal neurons is necessary for AKAP79/150 loss from spines and depolymerization of spine actin. Importantly, we demonstrate that NMDAR activation of PLC is also necessary for decreases in spine PSD95 levels and AMPAR internalization. Thus, PLC signaling is required for structural and functional changes in spine actin, PSD scaffolding, and AMPAR trafficking underlying postsynaptic expression of LTD.
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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.