Valproate is Neuroprotective Against Malonate Toxicity in Rat Striatum: An Association With Augmentation of High-Affinity Glutamate Uptake
The antiepileptic drug valproate (VPA) may be neuroprotective. We treated rats with VPA for 14 days (300 mg/kg twice daily) before intrastriatal injection of 1.5 μmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 ± 2 m...
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| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2004-11, Vol.24 (11), p.1226-1234 |
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| creator | Morland, Cecilie Boldingh, Karen Astrid Iversen, Evy Grini Hassel, Bjørnar |
| description | The antiepileptic drug valproate (VPA) may be neuroprotective. We treated rats with VPA for 14 days (300 mg/kg twice daily) before intrastriatal injection of 1.5 μmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 ± 2 mm3 versus 26 ± 8 mm3 (means ± SD; P = 10−4). Injection of NaCl that was equiosmolar with 1 M malonate caused lesions of only 1.2 ± 0.4 mm3 in control animals, whereas physiologic saline produced no lesion. VPA pretreatment reduced the malonate-induced extracellular accumulation of glutamate. This effect paralleled an increase in the striatal level of the glutamate transporter GLT, which augmented high-affinity glutamate uptake by 25%, as determined from the uptake of [3H] glutamate into striatal proteoliposomes. Malonate caused a 76% reduction in striatal adenosine triphosphate (ATP) content, but the glial, ATP-dependent formation of glutamine from radiolabeled glucose or glutamate was intact, indicating that glial ATP production supported uptake of glutamate. Striatal levels of HSP-70 and fos were reduced, and the levels of bcl-2 and phosphorylated extracellular signal-regulated kinase remained unaffected, but histone acetylation was increased by VPA treatment. The results suggest that augmentation of glutamate uptake may contribute importantly to VPA-mediated neuroprotection in striatum. |
| doi_str_mv | 10.1097/01.WCB.0000138666.25305.A7 |
| format | Article |
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We treated rats with VPA for 14 days (300 mg/kg twice daily) before intrastriatal injection of 1.5 μmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 ± 2 mm3 versus 26 ± 8 mm3 (means ± SD; P = 10−4). Injection of NaCl that was equiosmolar with 1 M malonate caused lesions of only 1.2 ± 0.4 mm3 in control animals, whereas physiologic saline produced no lesion. VPA pretreatment reduced the malonate-induced extracellular accumulation of glutamate. This effect paralleled an increase in the striatal level of the glutamate transporter GLT, which augmented high-affinity glutamate uptake by 25%, as determined from the uptake of [3H] glutamate into striatal proteoliposomes. Malonate caused a 76% reduction in striatal adenosine triphosphate (ATP) content, but the glial, ATP-dependent formation of glutamine from radiolabeled glucose or glutamate was intact, indicating that glial ATP production supported uptake of glutamate. Striatal levels of HSP-70 and fos were reduced, and the levels of bcl-2 and phosphorylated extracellular signal-regulated kinase remained unaffected, but histone acetylation was increased by VPA treatment. The results suggest that augmentation of glutamate uptake may contribute importantly to VPA-mediated neuroprotection in striatum.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1097/01.WCB.0000138666.25305.A7</identifier><identifier>PMID: 15545916</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Biological and medical sciences ; Biological Transport - drug effects ; Blood and lymphatic vessels ; Carbon Radioisotopes ; Cardiology. Vascular system ; Cell Death - drug effects ; Deoxyglucose - chemistry ; Deoxyglucose - metabolism ; Diseases of the aorta ; Dopamine - pharmacology ; Glutamic Acid - metabolism ; Histones - metabolism ; HSP70 Heat-Shock Proteins - metabolism ; Male ; Malonates - antagonists & inhibitors ; Malonates - chemistry ; Malonates - toxicity ; Medical sciences ; Mitogen-Activated Protein Kinases - metabolism ; Neostriatum - drug effects ; Neostriatum - pathology ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Neuropharmacology ; Neuroprotective agent ; Neuroprotective Agents - pharmacology ; Pharmacology. Drug treatments ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Proto-Oncogene Proteins c-fos - metabolism ; Rats ; Rats, Wistar ; Valproic Acid - pharmacology ; Vascular diseases and vascular malformations of the nervous system ; Weight Gain - drug effects</subject><ispartof>Journal of cerebral blood flow and metabolism, 2004-11, Vol.24 (11), p.1226-1234</ispartof><rights>2004 The International Society for Cerebral Blood Flow and Metabolism</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Nov 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-98a1fb088221a85c1a9b9cecaf409af3bed4844776fa876359acdca68c5705103</citedby><cites>FETCH-LOGICAL-c494t-98a1fb088221a85c1a9b9cecaf409af3bed4844776fa876359acdca68c5705103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1097/01.WCB.0000138666.25305.A7$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1097/01.WCB.0000138666.25305.A7$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21817,27922,27923,43619,43620</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16259415$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15545916$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morland, Cecilie</creatorcontrib><creatorcontrib>Boldingh, Karen Astrid</creatorcontrib><creatorcontrib>Iversen, Evy Grini</creatorcontrib><creatorcontrib>Hassel, Bjørnar</creatorcontrib><title>Valproate is Neuroprotective Against Malonate Toxicity in Rat Striatum: An Association With Augmentation of High-Affinity Glutamate Uptake</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>The antiepileptic drug valproate (VPA) may be neuroprotective. We treated rats with VPA for 14 days (300 mg/kg twice daily) before intrastriatal injection of 1.5 μmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 ± 2 mm3 versus 26 ± 8 mm3 (means ± SD; P = 10−4). Injection of NaCl that was equiosmolar with 1 M malonate caused lesions of only 1.2 ± 0.4 mm3 in control animals, whereas physiologic saline produced no lesion. VPA pretreatment reduced the malonate-induced extracellular accumulation of glutamate. This effect paralleled an increase in the striatal level of the glutamate transporter GLT, which augmented high-affinity glutamate uptake by 25%, as determined from the uptake of [3H] glutamate into striatal proteoliposomes. Malonate caused a 76% reduction in striatal adenosine triphosphate (ATP) content, but the glial, ATP-dependent formation of glutamine from radiolabeled glucose or glutamate was intact, indicating that glial ATP production supported uptake of glutamate. Striatal levels of HSP-70 and fos were reduced, and the levels of bcl-2 and phosphorylated extracellular signal-regulated kinase remained unaffected, but histone acetylation was increased by VPA treatment. The results suggest that augmentation of glutamate uptake may contribute importantly to VPA-mediated neuroprotection in striatum.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Transport - drug effects</subject><subject>Blood and lymphatic vessels</subject><subject>Carbon Radioisotopes</subject><subject>Cardiology. Vascular system</subject><subject>Cell Death - drug effects</subject><subject>Deoxyglucose - chemistry</subject><subject>Deoxyglucose - metabolism</subject><subject>Diseases of the aorta</subject><subject>Dopamine - pharmacology</subject><subject>Glutamic Acid - metabolism</subject><subject>Histones - metabolism</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Male</subject><subject>Malonates - antagonists & inhibitors</subject><subject>Malonates - chemistry</subject><subject>Malonates - toxicity</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Neostriatum - drug effects</subject><subject>Neostriatum - pathology</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Valproic Acid - pharmacology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Weight Gain - drug effects</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkd1u1DAQhS1ERZfCI4CsSlwm2En817uwghapBQlayp0167W3LtlksR1EX4GnxmlW7C2-sWb0zTljH4ROKSkpUeItoeXt8l1J8qG15JyXFasJK1vxBC0oY6oQhPKnaEEqQQsu5Pdj9DzG-8zLmrFn6DhDDVOUL9Cfb9DtwgDJYh_xJzuGIZfJmuR_WdxuwPcx4Svohn5iroff3vj0gH2Pv0DCX1PwkMbtGW573MY4mFz6oce3Pt3hdtxsbZ_mzuDwhd_cFa1zvp8kzrsxwXZSvdkl-GFfoCMHXbQv9_cJuvnw_np5UVx-Pv-4bC8L06gmFUoCdSsiZVVRkMxQUCtlrAHXEAWuXtl1I5tGCO5ACl4zBWZtgEvDBGGU1CfodNbND_052pj0_TCGPlvqiipWZ-EJOpshE4YYg3V6F_wWwoOmRE8paEJ1TkEfUtCPKehW5OHXe4dxtbXrw-j-2zPwZg9ANNC5AL3x8cDxiqmGssyJmYuwsYc1_2uFV_Nkjm0M9p-0evQn9V87Xqwy</recordid><startdate>20041101</startdate><enddate>20041101</enddate><creator>Morland, Cecilie</creator><creator>Boldingh, Karen Astrid</creator><creator>Iversen, Evy Grini</creator><creator>Hassel, Bjørnar</creator><general>SAGE Publications</general><general>Lippincott Williams & Wilkins</general><general>Sage Publications Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20041101</creationdate><title>Valproate is Neuroprotective Against Malonate Toxicity in Rat Striatum: An Association With Augmentation of High-Affinity Glutamate Uptake</title><author>Morland, Cecilie ; Boldingh, Karen Astrid ; Iversen, Evy Grini ; Hassel, Bjørnar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-98a1fb088221a85c1a9b9cecaf409af3bed4844776fa876359acdca68c5705103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Transport - drug effects</topic><topic>Blood and lymphatic vessels</topic><topic>Carbon Radioisotopes</topic><topic>Cardiology. Vascular system</topic><topic>Cell Death - drug effects</topic><topic>Deoxyglucose - chemistry</topic><topic>Deoxyglucose - metabolism</topic><topic>Diseases of the aorta</topic><topic>Dopamine - pharmacology</topic><topic>Glutamic Acid - metabolism</topic><topic>Histones - metabolism</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Male</topic><topic>Malonates - antagonists & inhibitors</topic><topic>Malonates - chemistry</topic><topic>Malonates - toxicity</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Neostriatum - drug effects</topic><topic>Neostriatum - pathology</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Valproic Acid - pharmacology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Weight Gain - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morland, Cecilie</creatorcontrib><creatorcontrib>Boldingh, Karen Astrid</creatorcontrib><creatorcontrib>Iversen, Evy Grini</creatorcontrib><creatorcontrib>Hassel, Bjørnar</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 Central (Corporate)</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>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>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Journal of cerebral blood flow and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morland, Cecilie</au><au>Boldingh, Karen Astrid</au><au>Iversen, Evy Grini</au><au>Hassel, Bjørnar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Valproate is Neuroprotective Against Malonate Toxicity in Rat Striatum: An Association With Augmentation of High-Affinity Glutamate Uptake</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2004-11-01</date><risdate>2004</risdate><volume>24</volume><issue>11</issue><spage>1226</spage><epage>1234</epage><pages>1226-1234</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract>The antiepileptic drug valproate (VPA) may be neuroprotective. We treated rats with VPA for 14 days (300 mg/kg twice daily) before intrastriatal injection of 1.5 μmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 ± 2 mm3 versus 26 ± 8 mm3 (means ± SD; P = 10−4). Injection of NaCl that was equiosmolar with 1 M malonate caused lesions of only 1.2 ± 0.4 mm3 in control animals, whereas physiologic saline produced no lesion. VPA pretreatment reduced the malonate-induced extracellular accumulation of glutamate. This effect paralleled an increase in the striatal level of the glutamate transporter GLT, which augmented high-affinity glutamate uptake by 25%, as determined from the uptake of [3H] glutamate into striatal proteoliposomes. Malonate caused a 76% reduction in striatal adenosine triphosphate (ATP) content, but the glial, ATP-dependent formation of glutamine from radiolabeled glucose or glutamate was intact, indicating that glial ATP production supported uptake of glutamate. Striatal levels of HSP-70 and fos were reduced, and the levels of bcl-2 and phosphorylated extracellular signal-regulated kinase remained unaffected, but histone acetylation was increased by VPA treatment. The results suggest that augmentation of glutamate uptake may contribute importantly to VPA-mediated neuroprotection in striatum.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>15545916</pmid><doi>10.1097/01.WCB.0000138666.25305.A7</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cerebral blood flow and metabolism, 2004-11, Vol.24 (11), p.1226-1234 |
| issn | 0271-678X 1559-7016 |
| language | eng |
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| subjects | Adenosine Triphosphate - metabolism Animals Biological and medical sciences Biological Transport - drug effects Blood and lymphatic vessels Carbon Radioisotopes Cardiology. Vascular system Cell Death - drug effects Deoxyglucose - chemistry Deoxyglucose - metabolism Diseases of the aorta Dopamine - pharmacology Glutamic Acid - metabolism Histones - metabolism HSP70 Heat-Shock Proteins - metabolism Male Malonates - antagonists & inhibitors Malonates - chemistry Malonates - toxicity Medical sciences Mitogen-Activated Protein Kinases - metabolism Neostriatum - drug effects Neostriatum - pathology Neurology Neurons - drug effects Neurons - metabolism Neurons - pathology Neuropharmacology Neuroprotective agent Neuroprotective Agents - pharmacology Pharmacology. Drug treatments Phosphorylation - drug effects Proto-Oncogene Proteins c-bcl-2 - metabolism Proto-Oncogene Proteins c-fos - metabolism Rats Rats, Wistar Valproic Acid - pharmacology Vascular diseases and vascular malformations of the nervous system Weight Gain - drug effects |
| title | Valproate is Neuroprotective Against Malonate Toxicity in Rat Striatum: An Association With Augmentation of High-Affinity Glutamate Uptake |
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