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Uptake, Metabolism, and Releasability of Ethyl Analogues of Homocholine by Rat Brain
Author(s) -
Welner S. A.,
Collier B.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12855.x
Subject(s) - acetylcholine , choline , acetylation , biochemistry , cerebral cortex , chemistry , stimulation , synaptosome , free nerve ending , metabolism , vesicle , cholinergic , in vitro , cytosol , biology , membrane , endocrinology , enzyme , gene
Ethyl analogues of homocholine were synthesized and used to describe further the specificities of the processes involved in choline uptake and acetylation and acetylcholine storage and release. Monoethylhomocholine, diethylhomocholine, and triethylhomocholine decreased the transport of choline into rat brain synaptosomes. The mono‐ and diethyl compounds were taken up into synaptosomes with similar affinity for the transport system as choline (5.8, 8.5, and 5.5 μ M , respectively) but at a somewhat slower rate (11.3, 8.5, and 37.3 nmol/g original tissue/h, respectively); the triethyl analogue was not transported at the concentrations tested, which further defines the structural specificity of the transport system. l ‐Carnitine did not affect the transport of the analogues. The in situ acetylation of mono‐ and diethyl‐homocholine by slices of rat cerebral cortex was measurable, but the in vitro acetylation by choline acetyl‐transferase solubilized from rat forebrain was not. Acetylation of the diethyl analogue by slices of cerebellar cortex was <20% of that by slices of cerebral cortex. Subcellular fractionation of cerebral slices showed that acetyldiethylhomocholine localized preferentially to the cytosolic rather than vesicular stores, indicating specificity of the mechanism responsible for the incorporation of acetylated product into the vesicles. The release of acetyldiethylhomocholine and of acetylcholine was tested from sliced brain that had been incubated with the precursors. Both esters were released spontaneously but stimulation with increased K + concentration enhanced the release of acetylcholine without changing the release of acetyldiethylhomocholine, suggesting that evoked transmitter release occurred from a vesicular store.