title: Diethylmaleate decreased ascorbic acid release induced by cerebral ischemia in cerebral cortex of the anesthetized rat.
abstract: The effect of diethylmaleate administration on ascorbic acid release following cerebral ischemia was investigated in anesthetized rat brain cortex. Cerebral ischemia, induced by ligating bilateral common carotid arteries and unilateral middle cerebral artery, significantly increased the extracellular ascorbic acid levels. Diethylmaleate (4 mmoles/kg, i.p.), which has been shown in earlier studies to decrease the ischemia-induced glutamate release, significantly reduced the ischemia-induced ascorbic acid release. The ischemia-induced ascorbic acid release was unaffected by perfusing NMDA receptor antagonist MK 801 (75 microM). Additionally, elevated extracellular glutamate levels, achieved by either externally applied glutamate solutions or by perfusing L-trans-pyrrolidine-2,4-dicarboxylate (PDC) (31.4 mM and 15.7 mM) to inhibit the glutamate uptake transporter, also significantly increased the extracellular ascorbic acid levels. These results suggested that ascorbic acid release in cerebral ischemia might be related to the elevated extracellular glutamate levels, which occurs following cerebral ischemia.
authors.affiliation: Department of Education and Research, Taichung Veterans General Hospital, Taiwan, ROC. csymdr@vghtc.vghtc.gov.tw
authors.forename: C S
authors.initials: CS
authors.lastname: Yang
authors.forename: P J
authors.initials: PJ
authors.lastname: Tsai
authors.forename: N N
authors.initials: NN
authors.lastname: Lin
authors.forename: J S
authors.initials: JS
authors.lastname: Kuo
mesh_terms: D027322:Amino Acid Transport System X-AG; D000758:Anesthesia; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D001923:Brain Chemistry / Q000187:drug effects; D002545:Brain Ischemia / Q000378:metabolism*; D002352:Carrier Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D003998:Dicarboxylic Acids / Q000494:pharmacology; D016291:Dizocilpine Maleate / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D050491:Glutamate Plasma Membrane Transport Proteins; D018698:Glutamic Acid / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism; D008297:Male; D008298:Maleates / Q000494:pharmacology*; D017551:Microdialysis; D014179:Neurotransmitter Uptake Inhibitors / Q000494:pharmacology; D011759:Pyrrolidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D027981:Symporters
chemical_list: D027322:Amino Acid Transport System X-AG; D002352:Carrier Proteins; D003998:Dicarboxylic Acids; D018691:Excitatory Amino Acid Antagonists; D050491:Glutamate Plasma Membrane Transport Proteins; D008298:Maleates; D014179:Neurotransmitter Uptake Inhibitors; D011759:Pyrrolidines; D016194:Receptors, N-Methyl-D-Aspartate; D027981:Symporters; D018698:Glutamic Acid; D016291:Dizocilpine Maleate; C083486:pyrrolidine-2,4-dicarboxylic acid; C014476:diethyl maleate; D005978:Glutathione; D001205:Ascorbic Acid