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Acetylcholine release from the rabbit isolated superior cervical ganglion preparation
Author(s) -
DAWES P. M.,
VIZI E. S.
Publication year - 1973
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.1476-5381.1973.tb06908.x
Subject(s) - acetylcholine , stimulation , superior cervical ganglion , endocrinology , medicine , physostigmine , chemistry , tetrodotoxin , phentolamine , ganglion , biology , anatomy
Summary1 . The rabbit isolated superior cervical ganglion preparation has been used to measure the release of acetylcholine from the tissue at rest and during preganglionic nerve stimulation. 2 . In the presence of physostigmine, the resting release of acetylcholine was 013+001 (nmol/g)/min (10 experiments) and that during stimulation with 300 shocks at 10 Hz was 3·1 ± 0·4 (pmol/g)/volley in 4 experiments (means ± s.e.m .). The volley output was independent of the frequency of stimulation over the range 1 to 10 Hz but was higher at 0·3 Hz. 3 . Tetrodotoxin, 0·8 μ m , had no effect on the resting release of acetylcholine but reduced the stimulated release below detectable levels (2 pmol). Lowering the temperature of the bathing fluid to 5° C reduced to below detectable levels both the resting release and that produced by nerve stimulation. 4 . The resting release of acetylcholine was increased by a potassium‐rich (49·4 m m K + ) bathing solution and by replacing the sodium chloride in the solution with lithium chloride (113 mM Li + ). 5 . (—)‐Noradrenaline bitartrate, 3 μ m , and (±)‐adrenaline bitartrate, 1·5 μ m , reduced by 70% the output of acetylcholine induced by stimulation at 0–3 Hz, but failed to reduce the resting release or that evoked by stimulation at 10 Hz. The inhibition was reversed by phentolamine. 6 . It is concluded that the rabbit superior cervical ganglion in vitro is a suitable preparation for studying transmitter release and that the ganglion blocking effect of catecholamines is due to a reduction in transmitter release.