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Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain
Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression...
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| Published in: | Journal of neuropathology and experimental neurology 1996-07, Vol.55 (7), p.832-840 |
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| Main Authors: | , , , , |
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| container_end_page | 840 |
| container_issue | 7 |
| container_start_page | 832 |
| container_title | Journal of neuropathology and experimental neurology |
| container_volume | 55 |
| creator | Gronlund, Kathryn M Gerhart, David Z Leino, Richard L Mccall, Anthony L Drewes, Lester R |
| description | Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immunocytochemical method and immunoblots to detect changes in the regional abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose utilization in normal brain. Following treatment with kainic acid and pentylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a region and isoform-specific manner. GLUT3 was maximal at eight hours, whereas GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight component of the GLUT3 doublet. The rapid response time for GLUT3 relative to GLUT1 may be related to the rapid increase in neuronal metabolic energy demands during seizure. These observations support the hypothesis that glucose transporters may be upregulated in brain under when brain glucose metabolism is elevated. |
| doi_str_mv | 10.1097/00005072-199607000-00008 |
| format | article |
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To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immunocytochemical method and immunoblots to detect changes in the regional abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose utilization in normal brain. Following treatment with kainic acid and pentylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a region and isoform-specific manner. GLUT3 was maximal at eight hours, whereas GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight component of the GLUT3 doublet. The rapid response time for GLUT3 relative to GLUT1 may be related to the rapid increase in neuronal metabolic energy demands during seizure. These observations support the hypothesis that glucose transporters may be upregulated in brain under when brain glucose metabolism is elevated.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/00005072-199607000-00008</identifier><identifier>PMID: 8965098</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Animals ; Biological and medical sciences ; Brain - drug effects ; Brain - metabolism ; Chronic Disease ; Glucose Transporter Type 1 ; Glucose Transporter Type 3 ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Immunoblotting ; Immunohistochemistry ; Kainic Acid - pharmacology ; Male ; Medical sciences ; Monosaccharide Transport Proteins - metabolism ; Nerve Tissue Proteins ; Nervous system (semeiology, syndromes) ; Neurology ; Pentylenetetrazole - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Seizures - metabolism ; Time Factors</subject><ispartof>Journal of neuropathology and experimental neurology, 1996-07, Vol.55 (7), p.832-840</ispartof><rights>1996 American Association of Neuropathologists, Inc</rights><rights>1996 INIST-CNRS</rights><rights>Copyright Lippincott Williams & Wilkins Jul 1996</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4928-7fccee7c372d75c49b53090ee96f2026ce746a5b2ecf1af399b884c16acbb38e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3171556$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8965098$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gronlund, Kathryn M</creatorcontrib><creatorcontrib>Gerhart, David Z</creatorcontrib><creatorcontrib>Leino, Richard L</creatorcontrib><creatorcontrib>Mccall, Anthony L</creatorcontrib><creatorcontrib>Drewes, Lester R</creatorcontrib><title>Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immunocytochemical method and immunoblots to detect changes in the regional abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose utilization in normal brain. Following treatment with kainic acid and pentylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a region and isoform-specific manner. GLUT3 was maximal at eight hours, whereas GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight component of the GLUT3 doublet. The rapid response time for GLUT3 relative to GLUT1 may be related to the rapid increase in neuronal metabolic energy demands during seizure. These observations support the hypothesis that glucose transporters may be upregulated in brain under when brain glucose metabolism is elevated.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Chronic Disease</subject><subject>Glucose Transporter Type 1</subject><subject>Glucose Transporter Type 3</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>Kainic Acid - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monosaccharide Transport Proteins - metabolism</subject><subject>Nerve Tissue Proteins</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Pentylenetetrazole - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Seizures - metabolism</subject><subject>Time Factors</subject><issn>0022-3069</issn><issn>1554-6578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqFkk1LAzEQhoMotVZ_grCIeFtNspuvY61aCwVB6zlk01m6dZutSZeiv97U1h4EMZchM09eZuYNQgnB1wQrcYPjYVjQlCjFsYi3dJOSB6hLGMtTzoQ8RF2MKU0zzNUxOglhHgmFVd5BHak4w0p20d1g5htX2eQFqs_WQ0hGznowAZJh3domxok3LiwbvwKf9IvWTY2zkFQueTar5Nabyp2io9LUAc52sYdeH-4ng8d0_DQcDfrj1OaKylSU1gIImwk6FSzmCpbFhgAULymm3ILIuWEFBVsSU2ZKFVLmlnBjiyKTkPXQ1VZ36Zv3FsJKL6pgoa6Ng6YNWkhCeU7lvyBhMo_SNIIXv8B503oXh9CUKonjnkSE5BayvgnBQ6mXvloY_6EJ1hs79I8dem_Hd2rTyPlOvy0WMN0_3O0_1i93dROsqcu4aluFPZYREe3kEcu32Lqpow3hrW7X4PUMTL2a6b8-Q_YF5cegWg</recordid><startdate>199607</startdate><enddate>199607</enddate><creator>Gronlund, Kathryn M</creator><creator>Gerhart, David Z</creator><creator>Leino, Richard L</creator><creator>Mccall, Anthony L</creator><creator>Drewes, Lester R</creator><general>American Association of Neuropathologists, Inc</general><general>Lippincott Williams & Wilkins</general><general>Oxford University Press</general><scope>IQODW</scope><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>K9.</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>199607</creationdate><title>Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain</title><author>Gronlund, Kathryn M ; Gerhart, David Z ; Leino, Richard L ; Mccall, Anthony L ; Drewes, Lester R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4928-7fccee7c372d75c49b53090ee96f2026ce746a5b2ecf1af399b884c16acbb38e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Chronic Disease</topic><topic>Glucose Transporter Type 1</topic><topic>Glucose Transporter Type 3</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>Kainic Acid - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monosaccharide Transport Proteins - metabolism</topic><topic>Nerve Tissue Proteins</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Pentylenetetrazole - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Seizures - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gronlund, Kathryn M</creatorcontrib><creatorcontrib>Gerhart, David Z</creatorcontrib><creatorcontrib>Leino, Richard L</creatorcontrib><creatorcontrib>Mccall, Anthony L</creatorcontrib><creatorcontrib>Drewes, Lester R</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>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gronlund, Kathryn M</au><au>Gerhart, David Z</au><au>Leino, Richard L</au><au>Mccall, Anthony L</au><au>Drewes, Lester R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>1996-07</date><risdate>1996</risdate><volume>55</volume><issue>7</issue><spage>832</spage><epage>840</epage><pages>832-840</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><notes>ObjectType-Article-1</notes><notes>ObjectType-Feature-2</notes><abstract>Pentylenetetrazole and kainic acid, seizure-inducing agents that are known to increase glucose utilization in brain, were used to produce chronic seizures in mature rats. To test the hypothesis that increased brain glucose utilization associated with seizures may alter glucose transporter expression, polyclonal carboxyl-terminal antisera to glucose transporters (GLUT1 and GLUT3) were employed with a quantitative immunocytochemical method and immunoblots to detect changes in the regional abundances of these proteins. GLUT3 abundances in control rats were found to be correlated with published values for regional glucose utilization in normal brain. Following treatment with kainic acid and pentylenetetrazole, both GLUT3 and GLUT1 increased in abundance in a region and isoform-specific manner. GLUT3 was maximal at eight hours, whereas GLUT1 was maximal at three days. Immunoblots indicated that most of the GLUT3 increase was accounted for by the higher molecular weight component of the GLUT3 doublet. The rapid response time for GLUT3 relative to GLUT1 may be related to the rapid increase in neuronal metabolic energy demands during seizure. These observations support the hypothesis that glucose transporters may be upregulated in brain under when brain glucose metabolism is elevated.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>8965098</pmid><doi>10.1097/00005072-199607000-00008</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of neuropathology and experimental neurology, 1996-07, Vol.55 (7), p.832-840 |
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| source | Oxford Journals - Connect here FIRST to enable access |
| subjects | Animals Biological and medical sciences Brain - drug effects Brain - metabolism Chronic Disease Glucose Transporter Type 1 Glucose Transporter Type 3 Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Immunoblotting Immunohistochemistry Kainic Acid - pharmacology Male Medical sciences Monosaccharide Transport Proteins - metabolism Nerve Tissue Proteins Nervous system (semeiology, syndromes) Neurology Pentylenetetrazole - pharmacology Rats Rats, Sprague-Dawley Reference Values Seizures - metabolism Time Factors |
| title | Chronic Seizures Increase Glucose Transporter Abundance in Rat Brain |
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