Present study was conducted to clarify the role of GABA in lidocaineinduced convulsion employing hippocampal slice.
Hippocampal slices(300400m) were prepared from hippocampal tissue blocks using a glass guide while the tissue was continuously moistened with oxygenated (95% 025% CO2) Krebsbicarbonate media (KB) at 37C. After prepartion, the slices were equilibrated for 1hr before biochemical testing in KB. Individual equilibrated slices were transferred to tissue holder, incubated for 5min in fresh oxygenated KB, and then exposed for 5min to 50mM K+ KB and transferred again to fresh KB for 30min rest period. Each slice served as its own control by exposing it a second time to 50mM K+ KB for 5min after the 30min rest and a second 5min incubation in fresh KB. After the 30min rest and a second 5min incubation in fresh KB, slices were transferred again to fresh KB containing 1, 2, 3, or 4mM lidocaine, incubated for 10min and then exposed to 50mM K+ KB+lidocaine solution for 5 min.
The results were as follows :
1. The release of GABA induced by the first and second 5min exposure of 50mM K+ was 95.917.28nmol and 80.613.04nmol, respectively. When compared with released amounts of GABA during the corresponding spontaneous periods, these were 4.7 and 4.9fold in-crease respectively and revealed that consecutive K+exposure increased GABA release with similar fashion.
2. The concentration of lidocaine necessary for 50 percent inhibition(ICso) of potassiuminduced release of GABA was 1.82mM.
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