S. Zini et al., EFFECT OF POTASSIUM CHANNEL MODULATORS ON THE RELEASE OF GLUTAMATE-INDUCED BY ISCHEMIC-LIKE CONDITIONS IN RAT HIPPOCAMPAL SLICES, Neuroscience letters, 153(2), 1993, pp. 202-205
The effects of the potassium channel openers lemakalim, RP 52891 and g
alanin and the Potassium channel blockers glibenclamide and gliquidone
were evaluated by the release of endogenous glutamate from rat hippoc
ampal slices subjected to a brief period of ischaemia (2-10 min). Isch
aemia was mimicked by incubating slices in a glucose free medium equil
ibrated with 95% N2/5% CO2. These conditions evoked a release of gluta
mate which was insensitive to tetrodotoxin and Ca2+ indicating a non-v
esicular origin. The release of glutamate evoked by a 6- or 8-min peri
od of ischaemia was reduced by 25-40% in the presence of lemakalim (10
muM), RP 52891 (10 muM) or galanin (0.3 muM), whereas it was enhanced
by 60 to 100% in the presence of glibenclamide (1 muM) and gliquidone
(2 muM). These observations suggest that cellular damage resulting fr
om ischaemia induced excessive release of glutamate in the hippocampus
may be partly reduced by potassium channel openers, and conversely in
creased by sulfonylureas.