STIMULATION OF ACETYLCHOLINE OUTPUT FROM BRAIN SLICES CAUSED BY THE IONOPHORES BrX‐537A AND A 23187

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Abstract
1 The effect of two ionophores, BrX-537A (Bromolasolacid) and A 23187, on acetylcholine (ACh) output from brain slices was studied. 2 The slices were prepared from rat cerebral cortex, incubated in Krebs solution containing physo-stigmine and ACh output determined by bioassay. 3 Both ionophores enhanced ACh output. BrX-537A exerted its maximal effect, a six fold increase, at a concentration of 1.8 μm, while A 23187 caused a three fold increase at a concentration of 58 um. 4 When the slices were incubated in a Ca-free medium, the effect of A 23187 on ACh output was abolished while that of BrX-537A was only reduced. BrX-537A was also active when disodium edetate (EDTA) was added to the Ca-free medium. 5 The activity of BrX-537A was not affected by the presence of tetrodotoxin in the incubation medium. 6 The stimulation of ACh output elicited by KC1 (25 him) was increased further by hyoscine, but not by BrX-537A. Hyoscine however had no effect when ACh output was stimulated by BrX-537A. 7 The effect of BrX-537A on ACh output was potentiated by the addition of Mg2+ (9.3 mm) to the incubation medium and was reduced in a Mg-free medium. 8 It is concluded that A 23187 stimulates ACh output by transporting extracellular Ca2+ into cholinergic nerve endings. The effect of BrX-537A does not depend only on Ca2+ but also on other mechanisms.