ArticlePloS one2009
NMDA receptor stimulation induces reversible fission of the neuronal endoplasmic reticulum.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Endoplasmic reticulum disruption stimulates nuclear membrane mechanotransduction.Nature cell biology · 2026Article
- Activation of Endoplasmic Reticulum-Localized Metabotropic Glutamate Receptor 5 (mGluBiomolecules · 2025Article
- The Endoplasmic Reticulum and Its Contacts: Emerging Roles in Axon Development, Neurotransmission, and Degeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Endoplasmic Reticulum in Metaplasticity: From Information Processing to Synaptic Proteostasis.Molecular neurobiology · 2022Review
- Retinal Glutamate Neurotransmission: From Physiology to Pathophysiological Mechanisms of Retinal Ganglion Cell Degeneration.Life (Basel, Switzerland) · 2022Review
- Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA?Developmental neurobiology · 2018Review
- Polybrene induces neural degeneration by bidirectional CaCell death & disease · 2018Article
- Advances in Plant ER Architecture and Dynamics.Plant physiology · 2018Review
- Mitochondrial Membrane Potential-dependent Endoplasmic Reticulum Fragmentation is an Important Step in Neuritic Degeneration.CNS neuroscience & therapeutics · 2016Article
- Extended Synaptotagmin (ESyt) Triple Knock-Out Mice Are Viable and Fertile without Obvious Endoplasmic Reticulum Dysfunction.PloS one · 2016Article
- ER morphology: sculpting with XendoU.Current biology : CB · 2014Article
- Rapid regulation of endoplasmic reticulum dynamics in dendritic spines by NMDA receptor activation.Molecular brain · 2014Article
- Transport along the dendritic endoplasmic reticulum mediates the trafficking of GABAB receptors.Journal of cell science · 2014Article
- Lipid dynamics at dendritic spines.Frontiers in neuroanatomy · 2014Review
- Fission and fusion of the neuronal endoplasmic reticulum.Translational stroke research · 2013Review
- Untangling the web: mechanisms underlying ER network formation.Biochimica et biophysica acta · 2013Review
- Cholesterol loss during glutamate-mediated excitotoxicity.The EMBO journal · 2012Article
- Emerging aspects of ER organization in root hair tip growth: lessons from RHD3 and Atlastin.Plant signaling & behavior · 2011Review
- Rapid fragmentation of the endoplasmic reticulum in cortical neurons of the mouse brain in situ following cardiac arrest.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
- Neuronal calcium homeostasis and dysregulation.Antioxidants & redox signaling · 2011Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With few exceptions the endoplasmic reticulum (ER) is considered a continuous system of endomembranes within which proteins and ions can move. We have studied dynamic structural changes of the ER in hippocampal neurons in primary culture and organotypic slices. Fluorescence recovery after photobleaching (FRAP) was used to quantify and model ER structural dynamics. Ultrastructure was assessed by electron microscopy. In live cell imaging experiments we found that, under basal conditions, the ER of neuronal soma and dendrites was continuous. The smooth and uninterrupted appearance of the ER changed dramatically after glutamate stimulation. The ER fragmented into isolated vesicles in a rapid fission reaction that occurred prior to overt signs of neuronal damage. ER fission was found to be independent of ER calcium levels. Apart from glutamate, the calcium ionophore ionomycin was able to induce ER fission. The N-methyl, D-aspartate (NMDA) receptor antagonist MK-801 inhibited ER fission induced by glutamate as well as by ionomycin. Fission was not blocked by either ifenprodil or kinase inhibitors. Interestingly, sub-lethal NMDA receptor stimulation caused rapid ER fission followed by fusion. Hence, ER fission is not strictly associated with cellular damage or death. Our results thus demonstrate that neuronal ER structure is dynamically regulated with important consequences for protein mobility and ER luminal calcium tunneling.
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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.