ArticleBiophysical journal2003
The invagination of excess surface area by shrinking neurons.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
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- The Role of Tau Proteoforms in Health and Disease.Molecular neurobiology · 2023Review
- Model of inverse bleb growth explains giant vacuole dynamics during cell mechanoadaptation.PNAS nexus · 2023Article
- An update to the Monro-Kellie doctrine to reflect tissue compliance after severe ischemic and hemorrhagic stroke.Scientific reports · 2020Article
- Weak protein-protein interactions in live cells are quantified by cell-volume modulation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Membrane reserves and hypotonic cell swelling.The Journal of membrane biology · 2006Article
- p38gamma regulates the localisation of SAP97 in the cytoskeleton by modulating its interaction with GKAP.The EMBO journal · 2005Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over most of their surface, neurons are surrounded by a narrow extracellular gap across which they make adhesive cell-cell contacts. Thus constrained, how do they regulate their geometry when osmotically perturbed? Specifically, are there any interesting consequences of local osmosis in such conditions? Using confocal imaging of shrinking neurons in culture, we observe water exiting into the cell-substratum gap. This water efflux generates a hydrostatic pressure that, at discrete (low adhesion) sites, causes the neuron's excess plasma membrane to invaginate, thus compensating for shrinkage with a pseudo-intracellular volume. To identify the minimal requirements of the process, a compartment/flux model was constructed. It comprises, essentially, a large liposome adhering in a labyrinthine fashion to a substratum. The model predicts that invaginations form at the cell-substratum interface under the influence of local osmosis, provided that adhesion across the gap is neither too tight nor too loose. Local osmosis in the central nervous system, in contrast to epithelia, is usually considered a mishap, not a physiological opportunity. We postulate, however, that local osmotic forces acting in conjunction with confined extracellular spaces could be harnessed in service of surface area, shape, and volume regulation when intense neural activity alters a neuron's osmotic balance.
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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.