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The effect of preganglionic nerve stimulation on the accumulation of certain analogues of choline by a sympathetic ganglion.
Author(s) -
Collier B,
Ilson D
Publication year - 1977
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1977.sp011679
Subject(s) - choline , stimulation , acetylcholine , chemistry , superior cervical ganglion , atropine , cholinergic , endocrinology , medicine , sympathetic ganglion , ganglion , biochemistry , biology , anatomy
1. Cat superior cervical ganglia were perfused with a Krebs solution containing 10(‐6) M [3H]homocholine (2‐hydroxypropyl‐trimethylammonium) or 10(‐5) M [14C]triethylcholine (2‐hydroxyethyl‐triethylammonium). Preganglionic nerve stimulation (20 Hz) increased the accumulation of homocholine (3‐2‐fold) and of triethylcholine (2‐1‐fold). This increased accumulation during stimulation was not the result of increased metabolism. 2. The increased accumulation of homocholine or triethylcholine induced by pregnaglionic nerve stimulation was not reduced by tubocurarine or by atropine, but it was blocked by choline and by hemicholinium. These results suggested that preganglionic nerve stimulation increased choline analogue accumulation into cholinergic nerve terminals. 3. The increased accumulation of homocholine or of triethylcholine induced by preganglionic nerve stimulation was reduced when the Ca2+ concentration was reduced and was abolished in the absence of Ca2+. However, changes in the Mg2+ concentration which depressed acetylcholine (ACh) release by amounts comparable to those induced by altered Ca2+ concentrations did not alter the uptake of homocholine or triethylcholine. It is concluded that the uptake of choline analogues is not regulated by transmitter release but that stimulation increases the uptake of the choline analogues by a Ca2+‐dependent mechanism. 4. The accumulation of ACh by ganglia perfused with a Krebs solution containing choline and high MgSO4 (18 mM) was measured. The ACh content of these ganglia did not increase, although choline transport presumably exceeded that necessary for ACh synthesis to replace released ACh. It is concluded that choline transport does not limit ACh synthesis in ganglia.