ReviewMolecular neurobiology2003
Molecular substrates of potassium spatial buffering in glial cells.
Review in Molecular neurobiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 39 citations in OpenAlex.
- Grey-box modeling and hypothesis testing of functional near-infrared spectroscopy-based cerebrovascular reactivity to anodal high-definition tDCS in healthy humans.PLoS computational biology · 2021Article
- Functional specialization of retinal Müller cell endfeet depends on an interplay between two syntrophin isoforms.Molecular brain · 2020Article
- The role of glial-specific Kir4.1 in normal and pathological states of the CNS.Acta neuropathologica · 2016Review
- Correlating Gene-specific DNA Methylation Changes with Expression and Transcriptional Activity of Astrocytic KCNJ10 (Kir4.1).Journal of visualized experiments : JoVE · 2015Article
- Molecular aspects of structure, gating, and physiology of pH-sensitive background K2P and Kir K+-transport channels.Physiological reviews · 2015Review
- Syntrophin proteins as Santa Claus: role(s) in cell signal transduction.Cellular and molecular life sciences : CMLS · 2013Review
- The impact of the glial spatial buffering on the K(+) Nernst potential.Cognitive neurodynamics · 2011Article
- Inwardly rectifying potassium channel Kir4.1 is responsible for the native inward potassium conductance of satellite glial cells in sensory ganglia.Neuroscience · 2010Article
- Signalling within the neurovascular unit in the mammalian retina.Experimental physiology · 2007Review
- In vivo measurement of brain extracellular space diffusion by cortical surface photobleaching.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Potassium buffering in the central nervous system.Neuroscience · 2004Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It is generally accepted that the foremost mechanism for the buffering of K+ from the extracellular space ([K+]o) in the brain is "K+ spatial buffering." This is the process by which glial cells dissipate local K+ gradients by transferring K+ ions from areas of high to low [K+]o. These glial K+ fluxes are mediated mainly by inwardly rectifying K+ (Kir) channels. The K+ spatial buffering hypothesis has been tested and confirmed in the retina, in which is has been termed as "K+ siphoning". In Müller cells, the primary glial cells of the retina, Kir channels are distributed in a highly non-uniform manner, exhibiting high concentrations in membrane domains facing the vitreous humor (endfeet) and in proximity to the blood vessels (perivascular processes). Such nonuniform distribution of Kir channels facilitates directed K+ fluxes in the retina from the synaptic plexiform layers to the vitreous humor and blood vessels. Recent molecular and electrophysiological studies in Müller cells have revealed a high degree of complexity in terms of Kir channel subunit composition, mechanisms of subcellular localization, and regulation. How such complexity fits into their proposed role in buffering [K+]o in retina is the main topic of this article.
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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.