Release of inhibitory neurotransmitters in response to anoxia in turtle brain
G. E. Nilsson and P. L. Lutz Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098. In mammals a massive release of the excitatory neurotransmitter glutamate, occurring within a few minutes of anoxia/ischemia, is thought to be a major mediator of anoxic brain d...
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Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1991-07, Vol.261 (1), p.32-R37 |
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container_issue | 1 |
container_start_page | 32 |
container_title | American journal of physiology. Regulatory, integrative and comparative physiology |
container_volume | 261 |
creator | Nilsson, G. E Lutz, P. L |
description | G. E. Nilsson and P. L. Lutz
Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098.
In mammals a massive release of the excitatory neurotransmitter glutamate,
occurring within a few minutes of anoxia/ischemia, is thought to be a major
mediator of anoxic brain damage. In contrast to the mammalian brain, the
turtle brain is exceptionally anoxia tolerant. Using intracerebral
microdialysis in turtle brain striatum, we have found a large increase in
the extracellular level of the inhibitory neurotransmitter
gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level
after 240 min, whereas no substantial release of glutamate occurred.
Moreover, the inhibitory neurotransmitters/neuromodulators glycine and
taurine also displayed increased extracellular levels during anoxia.
Increased extracellular levels of inhibitory amino acids may be one of the
hitherto elusive mechanisms that underlie the decreased activity and energy
consumption characterizing the anoxic turtle brain. |
doi_str_mv | 10.1152/ajpregu.1991.261.1.r32 |
format | Article |
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Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098.
In mammals a massive release of the excitatory neurotransmitter glutamate,
occurring within a few minutes of anoxia/ischemia, is thought to be a major
mediator of anoxic brain damage. In contrast to the mammalian brain, the
turtle brain is exceptionally anoxia tolerant. Using intracerebral
microdialysis in turtle brain striatum, we have found a large increase in
the extracellular level of the inhibitory neurotransmitter
gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level
after 240 min, whereas no substantial release of glutamate occurred.
Moreover, the inhibitory neurotransmitters/neuromodulators glycine and
taurine also displayed increased extracellular levels during anoxia.
Increased extracellular levels of inhibitory amino acids may be one of the
hitherto elusive mechanisms that underlie the decreased activity and energy
consumption characterizing the anoxic turtle brain.</description><identifier>ISSN: 0363-6119</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.1991.261.1.r32</identifier><identifier>PMID: 1677540</identifier><language>eng</language><publisher>United States</publisher><subject>Alanine - metabolism ; Animals ; Brain - metabolism ; Dialysis - methods ; Electrophysiology ; Extracellular Space - metabolism ; gamma-Aminobutyric Acid - metabolism ; Glycine - metabolism ; Hypoxia - metabolism ; Hypoxia - physiopathology ; Neural Inhibition - physiology ; Neurotransmitter Agents - metabolism ; Potassium - pharmacology ; Taurine - metabolism ; Turtles - metabolism</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 1991-07, Vol.261 (1), p.32-R37</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c343t-6fba4c03a36f901b33a1b8ad6bfdac34e6526cf6c2589cac143ef11dbe4b1a7c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1677540$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nilsson, G. E</creatorcontrib><creatorcontrib>Lutz, P. L</creatorcontrib><title>Release of inhibitory neurotransmitters in response to anoxia in turtle brain</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol</addtitle><description>G. E. Nilsson and P. L. Lutz
Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098.
In mammals a massive release of the excitatory neurotransmitter glutamate,
occurring within a few minutes of anoxia/ischemia, is thought to be a major
mediator of anoxic brain damage. In contrast to the mammalian brain, the
turtle brain is exceptionally anoxia tolerant. Using intracerebral
microdialysis in turtle brain striatum, we have found a large increase in
the extracellular level of the inhibitory neurotransmitter
gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level
after 240 min, whereas no substantial release of glutamate occurred.
Moreover, the inhibitory neurotransmitters/neuromodulators glycine and
taurine also displayed increased extracellular levels during anoxia.
Increased extracellular levels of inhibitory amino acids may be one of the
hitherto elusive mechanisms that underlie the decreased activity and energy
consumption characterizing the anoxic turtle brain.</description><subject>Alanine - metabolism</subject><subject>Animals</subject><subject>Brain - metabolism</subject><subject>Dialysis - methods</subject><subject>Electrophysiology</subject><subject>Extracellular Space - metabolism</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Glycine - metabolism</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - physiopathology</subject><subject>Neural Inhibition - physiology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Potassium - pharmacology</subject><subject>Taurine - metabolism</subject><subject>Turtles - metabolism</subject><issn>0363-6119</issn><issn>0002-9513</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkF1LwzAUhoMoc05_gtIrr2zNadpsvRTxCybC0OuQZKdbRtfUJEX7783YcFcHzvsFDyE3QDOAMr-Xm87hqs-gqiDLOWSQOZafkHEU8xSKip6SMWWcpRygOicX3m8opQUr2IiMgE-nZUHH5H2BDUqPia0T066NMsG6IWmxdzY42fqtCQGdj2Li0He2jd5gE9naXyN339C70GCinDTtJTmrZePx6nAn5Ov56fPxNZ1_vLw9PsxTHedDymslC02ZZLyuKCjGJKiZXHJVL2W0IC9zrmuu83JWaamhYFgDLBUWCuRUswm53fd2zn736IPYGq-xaWSLtvdiRqe05DOIRr43ame9d1iLzpmtdIMAKnYcxYGj2HEUkaMAsWB5DF4fFnq1xeUxtgcX9bu9vjar9Y9xKLr14I1t7Gr47zzW_QFs14M5</recordid><startdate>19910701</startdate><enddate>19910701</enddate><creator>Nilsson, G. E</creator><creator>Lutz, P. L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19910701</creationdate><title>Release of inhibitory neurotransmitters in response to anoxia in turtle brain</title><author>Nilsson, G. E ; Lutz, P. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c343t-6fba4c03a36f901b33a1b8ad6bfdac34e6526cf6c2589cac143ef11dbe4b1a7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Alanine - metabolism</topic><topic>Animals</topic><topic>Brain - metabolism</topic><topic>Dialysis - methods</topic><topic>Electrophysiology</topic><topic>Extracellular Space - metabolism</topic><topic>gamma-Aminobutyric Acid - metabolism</topic><topic>Glycine - metabolism</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - physiopathology</topic><topic>Neural Inhibition - physiology</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Potassium - pharmacology</topic><topic>Taurine - metabolism</topic><topic>Turtles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nilsson, G. E</creatorcontrib><creatorcontrib>Lutz, P. L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nilsson, G. E</au><au>Lutz, P. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Release of inhibitory neurotransmitters in response to anoxia in turtle brain</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1991-07-01</date><risdate>1991</risdate><volume>261</volume><issue>1</issue><spage>32</spage><epage>R37</epage><pages>32-R37</pages><issn>0363-6119</issn><issn>0002-9513</issn><eissn>1522-1490</eissn><abstract>G. E. Nilsson and P. L. Lutz
Rosenstiel School of Marine and Atmospheric Science, University of Miami, Florida 33149-1098.
In mammals a massive release of the excitatory neurotransmitter glutamate,
occurring within a few minutes of anoxia/ischemia, is thought to be a major
mediator of anoxic brain damage. In contrast to the mammalian brain, the
turtle brain is exceptionally anoxia tolerant. Using intracerebral
microdialysis in turtle brain striatum, we have found a large increase in
the extracellular level of the inhibitory neurotransmitter
gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level
after 240 min, whereas no substantial release of glutamate occurred.
Moreover, the inhibitory neurotransmitters/neuromodulators glycine and
taurine also displayed increased extracellular levels during anoxia.
Increased extracellular levels of inhibitory amino acids may be one of the
hitherto elusive mechanisms that underlie the decreased activity and energy
consumption characterizing the anoxic turtle brain.</abstract><cop>United States</cop><pmid>1677540</pmid><doi>10.1152/ajpregu.1991.261.1.r32</doi></addata></record> |
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language | eng |
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source | MEDLINE; Alma/SFX Local Collection |
subjects | Alanine - metabolism Animals Brain - metabolism Dialysis - methods Electrophysiology Extracellular Space - metabolism gamma-Aminobutyric Acid - metabolism Glycine - metabolism Hypoxia - metabolism Hypoxia - physiopathology Neural Inhibition - physiology Neurotransmitter Agents - metabolism Potassium - pharmacology Taurine - metabolism Turtles - metabolism |
title | Release of inhibitory neurotransmitters in response to anoxia in turtle brain |
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