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The release of acetylcholine by acetylcholine in the cat's superior cervical ganglion
Author(s) -
COLLIER B.,
KATZ H. S.
Publication year - 1970
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.1476-5381.1970.tb12905.x
Subject(s) - acetylcholine , carbachol , superior cervical ganglion , stimulation , chemistry , ganglion , free nerve ending , endocrinology , medicine , cholinergic , anatomy , biology
Summary1 The experiments described in this paper tested the effect of acetylcholine (ACh), carbachol or preganglionic nerve stimulation on the release of ACh from the cat's perfused superior cervical ganglion; radioactive tracer methods were used. 2 When the ganglion's transmitter store of ACh had been labelled, radioactive ACh was released by nerve stimulation (5 Hz for 2 min), but there was no release by ACh (0.15–15 μg) or by carbachol (1–10 μg) when these drugs were injected close to the ganglion. Perfusion with low or moderate concentrations of ACh (015–5 μg/ml) also failed to release ACh, but high concentrations (15–50 μg/ml) released a small amount of labelled material. There was no correlation between ganglion stimulation by ACh and release of radioactivity. 3 Ganglion‐blocking concentrations of ACh did not reduce the release of ACh during continuous nerve stimulation. 4 When resting (unstimulated) ganglia were perfused with 3 H‐choline and eserine, the extra ACh synthesized and stored by such ganglia (surplus ACh) was labelled. Preganglionic nerve stimulation (5 Hz for 2 min) did not release surplus ACh, but perfusion with ACh (0.5–15 μg/ml), or injection of carbachol (0.5–2.5 μg) did. 5 Surplus ACh released by ACh or by carbachol did not contribute to the ganglion stimulating effect of either drug. 6 It is concluded that the presynaptic effects of ACh are not of physiological importance.