{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:22:34Z","timestamp":1777792954614,"version":"3.51.4"},"reference-count":45,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2004,11,1]],"date-time":"2004-11-01T00:00:00Z","timestamp":1099267200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p>\n                    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 \u03bcmol (1 M) of the succinate dehydrogenase inhibitor malonate. VPA-treated animals developed smaller lesions than control animals: 10 \u00b1 2 mm\n                    <jats:sup>3<\/jats:sup>\n                    versus 26 \u00b1 8 mm\n                    <jats:sup>3<\/jats:sup>\n                    (means \u00b1 SD; P = 10\n                    <jats:sup>\u22124<\/jats:sup>\n                    ). Injection of NaCl that was equiosmolar with 1 M malonate caused lesions of only 1.2 \u00b1 0.4 mm\n                    <jats:sup>3<\/jats:sup>\n                    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 [\n                    <jats:sup>3<\/jats:sup>\n                    H] 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.\n                  <\/jats:p>","DOI":"10.1097\/01.wcb.0000138666.25305.a7","type":"journal-article","created":{"date-parts":[[2004,11,1]],"date-time":"2004-11-01T04:02:30Z","timestamp":1099281750000},"page":"1226-1234","source":"Crossref","is-referenced-by-count":38,"title":["Valproate is Neuroprotective against Malonate Toxicity in Rat Striatum: An Association with Augmentation of High-Affinity Glutamate Uptake"],"prefix":"10.1177","volume":"24","author":[{"given":"Cecilie","family":"Morland","sequence":"first","affiliation":[{"name":"Norwegian Defense Research Establishment, Kjeller, Norway"}]},{"given":"Karen Astrid","family":"Boldingh","sequence":"additional","affiliation":[{"name":"Norwegian Defense Research Establishment, Kjeller, Norway"}]},{"given":"Evy Grini","family":"Iversen","sequence":"additional","affiliation":[{"name":"Norwegian Defense 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