Energetics of functional activation in neural tissues
Glucose utilization (ICMRglc) increases linearly with spike frequency in neuropil but not perikarya of functionally activated neural tissues. Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates ICMRglc in neural tissues; these increase...
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| Veröffentlicht in: | Neurochemical research 1999-02, Vol.24 (2), p.321-329 |
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| creator | SOKOLOFF, L |
| description | Glucose utilization (ICMRglc) increases linearly with spike frequency in neuropil but not perikarya of functionally activated neural tissues. Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates ICMRglc in neural tissues; these increases are blocked by ouabain, an inhibitor of Na+,K+-ATPase. Stimulating Na+,K+-ATPase activity to restore ionic gradients degraded by enhanced spike activity appears to trigger these increases in ICMRglc. Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased ICMRglc. ICMRglc in cultured astroglia is unaffected by elevated [K+]o but is stimulated by increased intracellular [Na+] ([Na+]i), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates ICMRglc in astroglia. This effect is unaffected by inhibitors of NMDA or non-NMDA receptors, blocked by ouabain, and absent in Na+-free medium; it appears to be mediated by increased [Na+]i due to combined uptake of Na+ with glutamate via Na+/glutamate co-transporters. |
| doi_str_mv | 10.1023/a:1022534709672 |
| format | Article |
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Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates ICMRglc in neural tissues; these increases are blocked by ouabain, an inhibitor of Na+,K+-ATPase. Stimulating Na+,K+-ATPase activity to restore ionic gradients degraded by enhanced spike activity appears to trigger these increases in ICMRglc. Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased ICMRglc. ICMRglc in cultured astroglia is unaffected by elevated [K+]o but is stimulated by increased intracellular [Na+] ([Na+]i), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates ICMRglc in astroglia. 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Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates ICMRglc in neural tissues; these increases are blocked by ouabain, an inhibitor of Na+,K+-ATPase. Stimulating Na+,K+-ATPase activity to restore ionic gradients degraded by enhanced spike activity appears to trigger these increases in ICMRglc. Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased ICMRglc. ICMRglc in cultured astroglia is unaffected by elevated [K+]o but is stimulated by increased intracellular [Na+] ([Na+]i), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates ICMRglc in astroglia. This effect is unaffected by inhibitors of NMDA or non-NMDA receptors, blocked by ouabain, and absent in Na+-free medium; it appears to be mediated by increased [Na+]i due to combined uptake of Na+ with glutamate via Na+/glutamate co-transporters.</description><subject>Action Potentials</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Energy Metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>General aspects. Models. 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Methods</topic><topic>Glucose - metabolism</topic><topic>Neuropil - metabolism</topic><topic>Neuropil - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SOKOLOFF, L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SOKOLOFF, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Energetics of functional activation in neural tissues</atitle><jtitle>Neurochemical research</jtitle><addtitle>Neurochem Res</addtitle><date>1999-02-01</date><risdate>1999</risdate><volume>24</volume><issue>2</issue><spage>321</spage><epage>329</epage><pages>321-329</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><coden>NEREDZ</coden><abstract>Glucose utilization (ICMRglc) increases linearly with spike frequency in neuropil but not perikarya of functionally activated neural tissues. Electrical stimulation, increased extracellular [K+] ([K+]o), or opening of Na+ channels with veratridine stimulates ICMRglc in neural tissues; these increases are blocked by ouabain, an inhibitor of Na+,K+-ATPase. Stimulating Na+,K+-ATPase activity to restore ionic gradients degraded by enhanced spike activity appears to trigger these increases in ICMRglc. Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased ICMRglc. ICMRglc in cultured astroglia is unaffected by elevated [K+]o but is stimulated by increased intracellular [Na+] ([Na+]i), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates ICMRglc in astroglia. This effect is unaffected by inhibitors of NMDA or non-NMDA receptors, blocked by ouabain, and absent in Na+-free medium; it appears to be mediated by increased [Na+]i due to combined uptake of Na+ with glutamate via Na+/glutamate co-transporters.</abstract><cop>New York, NY</cop><pub>Springer</pub><pmid>9972882</pmid><doi>10.1023/a:1022534709672</doi><tpages>9</tpages></addata></record> |
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| subjects | Action Potentials Animals Biological and medical sciences Energy Metabolism Fundamental and applied biological sciences. Psychology General aspects. Models. Methods Glucose - metabolism Neuropil - metabolism Neuropil - physiology Vertebrates: nervous system and sense organs |
| title | Energetics of functional activation in neural tissues |
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