Kainic acid (KA)-induced seizures in Sprague-Dawley rats and the effect of dietary taurine (TAU) supplementation or deficiency

Male Sprague-Dawley rats received TAU supplementation (1.5% in drinking water) or TAU deficient diets for 4 weeks to test for a possible neuroprotective role of TAU in KA-induced (10 mg/kg s.c.) seizures. TAU supplementation significantly increased serum and hippocampal TAU levels, but not TAU conte...

Full description

Saved in:
Bibliographic Details
Published in:Amino acids 1999-01, Vol.16 (2), p.133-147
Main Authors: Eppler, B, Patterson, T A, Zhou, W, Millard, W J, Dawson, Jr, R
Format: Article
Language:English
Subjects:
Amino acids
Amino Acids - analysis
Animals
Anticonvulsants - pharmacology
Attenuation
Binding sites
Body Weight - drug effects
Brain Chemistry - drug effects
Catecholamines - analysis
Cortexes
Diet
Diets
Excitatory Amino Acid Agonists - pharmacology
Kainic Acid - pharmacology
Male
Rats
Rats, Sprague-Dawley
Rodents
Seizures
Seizures - chemically induced
Seizures - drug therapy
Seizures - prevention & control
Serums
Taurine - deficiency
Taurine - pharmacology
Temporal logic
Time Factors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Male Sprague-Dawley rats received TAU supplementation (1.5% in drinking water) or TAU deficient diets for 4 weeks to test for a possible neuroprotective role of TAU in KA-induced (10 mg/kg s.c.) seizures. TAU supplementation significantly increased serum and hippocampal TAU levels, but not TAU content in temporal cortex or striatum. TAU deficient diets did not attenuate serum or tissue TAU levels. Dietary TAU supplementation failed to decrease the number or latency of partial or clonic-tonic seizures or wet dog shakes, whereas a TAU deficient diet decreased the number of clonictonic and partial seizures. This study does not support previous observations of an anticonvulsant effect of TAU against KA-induced seizures. KA-treatment decreased alpha 2-adrenergic receptor binding sites and TAU content in the temporal cortex across all dietary treatment groups, supporting previous evidence of severe KA-induced damage and neuronal loss in this brain region.
ISSN:0939-4451
1438-2199
DOI:10.1007/BF01321532