NDLI: Seizure-induced changes in energy metabolites and effects of N-tert-butyl-α-phenylnitrone (PNB) and vitamin E in rats

Content Provider	Springer Nature Link
Author	Gupta, Ramesh C. Milatovic, Dejan Zivin, Marko Dettbarn, Wolf D.
Copyright Year	2000
Abstract	Impaired energy metabolism may play a critical role in the neuronal injury caused by kainic acid (KA) induced status epilepticus (SE). Following an acute dose of KA (15 mg/kg, sc) rats developed SE within 1 h. Rats were sacrificed 1 or 72 h after the onset of SE using a head focused microwave technique and the brain regions (pyriform cortex, amygdala, and hippocampus) were assayed for energy metabolites: ATP, ADP, AMP, phosphocreatine (PCr) and creatine (Cr) using reversed-phase HPLC (RP-HPLC). Control values were significantly higher in cortex (23-32%) than in other brain regions. Within 1 h, SE caused a marked decline in ATP (44-56%), PCr (49-64%), total adenine nucleotides (TAN, 45-50%) and total creatine compounds (TCC, 32-51%). Within three days, the hippocampus showed the greatest recovery, as the reduced values returned to normal. Pretreatment of rats with an antioxidant (PBN, 200 mg/kg, ip, 30 min prior to KA; or vitamin E (Vit-E), 100 mg/kg, ip/day for 3 days), which did not prevent seizure activity, attenuated depletion of high-energy phosphates caused by KA. These findings suggest that the depletion of energy metabolites caused by KA-induced seizures may be linked to oxidative stress mediated toxicity.
Starting Page	R160
Ending Page	R162
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	440
Issue Number	1
e-ISSN	14322013
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2016-10-27
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Human Physiology Molecular Medicine Neurosciences Cell Biology Receptors
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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