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STIMULATION OF ACETYLCHOLINE OUTPUT FROM BRAIN SLICES CAUSED BY THE IONOPHORES BrX‐537A AND A 23187
Author(s) -
CASAMENTI F.,
MANTOVANI P.,
PEPEU G.
Publication year - 1978
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1978.tb09755.x
Subject(s) - chemistry , acetylcholine , physostigmine , stimulation , cholinergic , tetrodotoxin , incubation , atropine , extracellular , free nerve ending , biophysics , pharmacology , biochemistry , medicine , biology
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 μ m , 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 Mg 2+ (9.3 m m ) 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 Ca 2+ into cholinergic nerve endings. The effect of BrX‐537A does not depend only on Ca 2+ but also on other mechanisms.