ArticleMolecular pharmacology2009
Phosphatidylinositol (4,5)-bisphosphate regulation of N-methyl-D-aspartate receptor channels in cortical neurons.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Implicates of PIP5K1α in asthma-related biological processes: insights into mechanisms and therapeutic potential.Journal of translational medicine · 2025Review
- Altered GM1 catabolism affects NMDAR-mediated CaCell reports · 2024Article
- Article
- Signaling pathways involved in NMDA-induced suppression of M-channels in corticotropin-releasing hormone neurons in central amygdala.Journal of neurochemistry · 2022Article
- Mice Deficient inMolecular and cellular biology · 2017Article
- Identification of postsynaptic phosphatidylinositol-4,5-bisphosphate (PIPScientific reports · 2017Article
- Phosphoinositide control of membrane protein function: a frontier led by studies on ion channels.Annual review of physiology · 2015Review
- Structural basis of PI(4,5)P2-dependent regulation of GluA1 by phosphatidylinositol-5-phosphate 4-kinase, type II, alpha (PIP5K2A).Pflugers Archiv : European journal of physiology · 2014Article
- Phosphatidylinositol 4,5-bisphosphate depletion fails to affect neurosteroid modulation of GABAA receptor function.Psychopharmacology · 2014Article
- Shank3 deficiency induces NMDA receptor hypofunction via an actin-dependent mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Phosphoinositides: tiny lipids with giant impact on cell regulation.Physiological reviews · 2013Review
- Reduction of synaptojanin 1 ameliorates synaptic and behavioral impairments in a mouse model of Alzheimer's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Dual effect of phosphatidylinositol (4,5)-bisphosphate PIP(2) on Shaker K(+) [corrected] channels.The Journal of biological chemistry · 2012Article
- Phosphatidylinositol-4,5-bisphosphate regulates epidermal growth factor receptor activation.Pflugers Archiv : European journal of physiology · 2011Article
- Channelopathies linked to plasma membrane phosphoinositides.Pflugers Archiv : European journal of physiology · 2010Review
- Ca(2+) channels on the move.Biochemistry · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The membrane phospholipid phosphatidylinositol (4,5)-bisphosphate (PIP(2)) has been implicated in the regulation of several ion channels and transporters. In this study, we examined the impact of PIP(2) on N-methyl-D-aspartate receptors (NMDARs) in cortical neurons. Blocking PIP(2) synthesis by inhibiting phosphoinositide-4 kinase, or stimulating PIP(2) hydrolysis via activation of phospholipase C (PLC), or blocking PIP(2) function with an antibody caused a significant reduction of NMDAR-mediated currents. On the other hand, inhibition of PLC or application of PIP(2) caused an enhancement of NMDAR currents. These electrophysiological effects were accompanied by changes in NMDAR surface clusters induced by agents that manipulate PIP(2) levels. The PIP(2) regulation of NMDAR currents was abolished by the dynamin inhibitory peptide, which blocks receptor internalization. Agents perturbing actin stability prevented PIP(2) regulation of NMDAR currents, suggesting the actin-dependence of this effect of PIP(2). Cofilin, a major actin depolymerizing factor, which has a common binding sequence for actin and PIP(2), was required for PIP(2) regulation of NMDAR currents. It is noteworthy that the PIP(2) regulation of NMDAR channels was impaired in a transgenic mouse model of Alzheimer's disease, probably because of the amyloid-beta disruption of PIP(2) metabolism. Taken together, our data suggest that continuous synthesis of PIP(2) at the membrane might be important for the maintenance of NMDARs at the cell surface. When PIP(2) is lost, cofilin is released from the PIP(2) complex and is rendered free to depolymerize actin. With the actin cytoskeleton no longer intact, NMDARs are internalized via a dynamin/clathrin-dependent mechanism, leading to reduced NMDAR currents.
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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.