GABA induced changes in acetylcholine release from slices of guinea-pig brain
- 1 January 1982
- journal article
- research article
- Published by Springer Nature in Naunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie
- Vol. 318 (4), 253-258
- https://doi.org/10.1007/bf00501162
Abstract
Summary The effect of GABA on acetylcholine (ACh) release was investigated on superfused slices of guinea-pig cerebral cortex (CC), caudate nucleus (CN), tuberculum olfactorium and brain stem. GABA (1–6×10−3 mol/l) increased the spontaneous and KCl-evoked ACh overflow in CC and CN, reduced the electrically-evoked release in all areas tested (most evidently in CC and CN) and lowered the threshold of electric stimulation-induced ACh release in CC. These effects were also caused by 3-amino-1-propane sulphonic acid (1×10−3mol/l) and ethanolamine-O-sulphate (2×10−4mol/l), were reduced by bicuculline (1×10−4mol/l) and fully antagonized by picrotoxin (8×10−5mol/l), but they were not influenced by phentolamine, methysergide, spiroperidol or strychnine. Tetrodotoxin (TTX) (5×10−7mol/l) blocked the facilitation of spontaneous ACh release by GABA only when the slices were perfused with normal Krebs solution, but not when perfused with a KCl-enriched medium. These results suggest that GABA affects the cholinergic transmitter release through bicuculline- and picrotoxin-sensitive receptors, showing low affinity toward the agonist. Moreover GABA modulation of resting ACh release requires action potentials only in normal [K+]0, but not in high [K+]0, suggesting that GABA-receptive sites are located at cholinergic terminals.Keywords
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