Premium
Effects of Taurine and Glycine on Epileptiform Activity Induced by Removal of Mg 2+ in Combined Rat Entorhinal Cortex–Hippocampal Slices
Author(s) -
Kirchner Anne,
Breustedt Jorg,
Rosche Berit,
Heinemann Uwe F.,
Schmieden Volker
Publication year - 2003
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2003.01603.x
Subject(s) - strychnine , glycine receptor , entorhinal cortex , glycine , taurine , neocortex , chemistry , hippocampus , inhibitory postsynaptic potential , hippocampal formation , neuroscience , epileptogenesis , extracellular , biochemistry , biology , amino acid
Summary: Purpose: The imbalance between neuronal inhibition and excitation contributes to epileptogenesis. Inhibition in the central nervous system (CNS) is mediated by γ‐aminobutyric acid (GABA) and glycine. Recent studies indicate the expression of glycine receptor (GlyR) in hippocampus and neocortex. However, the function of GlyR in these regions is not clarified completely. The aim of this study was to investigate whether the GlyR agonists glycine and taurine promote an anticonvulsive effect. Methods: We induced epileptiform discharges by reducing extracellular Mg 2+ concentration in combined rat entorhinal cortex–hippocampal slices (400 μm). Epileptiform discharges were detected by using extracellular recording techniques. Results: Seizure‐like events were suppressed by taurine, exhibiting a half‐maximal inhibitory effect (IC 50 ) of 0.9 m M . Suppression of late recurrent discharges in the medial entorhinal cortex and recurrent short discharges in the hippocampus was obtained at an IC 50 value of 1.6 and 2.1 m M , respectively. Strychnine at concentrations <1 μ M abolished these effects. Likewise glycine, after an initial proconvulsant effect, suppressed epileptiform discharges. Conclusions: These findings show that GlyR agonists, in particular taurine, could serve as potential anticonvulsants and suggest an important role of GlyR in cortical function and dysfunction.