KAINIC ACID CAUSES REDOX CHANGES IN CEREBRAL-CORTEX EXTRACELLULAR FLUID - NMDA RECEPTOR ACTIVITY INCREASES ASCORBIC-ACID WHEREAS SEIZURE ACTIVITY INCREASES URIC-ACID

Citation
Me. Layton et al., KAINIC ACID CAUSES REDOX CHANGES IN CEREBRAL-CORTEX EXTRACELLULAR FLUID - NMDA RECEPTOR ACTIVITY INCREASES ASCORBIC-ACID WHEREAS SEIZURE ACTIVITY INCREASES URIC-ACID, Neuropharmacology, 37(2), 1998, pp. 149-157
Citations number
68
Categorie Soggetti
Pharmacology & Pharmacy",Neurosciences
Journal title
ISSN journal
00283908
Volume
37
Issue
2
Year of publication
1998
Pages
149 - 157
Database
ISI
SICI code
0028-3908(1998)37:2<149:KACRCI>2.0.ZU;2-#
Abstract
Kainic acid (KA) causes seizures and extensive brain damage in rats. T o study the effects of KA on the redox state in cerebral cortex extrac ellular fluid (ECF), ascorbic and uric acid concentrations were measur ed in intracerebral microdialysis samples before and after systemic KA administration (ip). During seizures, concentrations of ascorbic and uric acid increased 500 and 100%, respectively. When midazolam was giv en with KA to prevent seizures, ascorbic acid still increased 400%, bu t uric acid increased only transiently. When the NMDA receptor antagon ist aminophosphonovaleric acid (APV) was included in the microdialysis perfusion media, ascorbic acid levels decreased during baseline perfu sion in a concentration-dependent manner. APV then suppressed the KA-i nduced increase in ascorbic acid levels, without blocking seizure acti vity. In summary, increased uric acid levels in brain ECF activity aft er KA administration are related to the induced seizure, but ascorbic acid levels are associated with NMDA receptor activity. (C) 1995 Elsev ier Science Ltd. All rights reserved.