23 research outputs found
Comparison of the Muscarinic Receptor Binding Activity of Some Tertiary Amines and Their Quaternary Ammonium Analogues
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Free and bound choline blood levels after phosphatidylcholine
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/110000/1/cptclpt198264.pd
Spontaneous Regeneration of Free Muscarinic Receptor after Alkylation by BM 123. II. Recovery in Broken Cell Preparations1
ABSTRAC
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Synaptosomal transport and acetylation of choline
Acetylcholine (ACh) synthesis can be impaired by reduction of the availability of either of its precursors, choline (Ch) or acetylcoenzyme A (AcCoA). The high affinity transport of Ch is inhibited by hemicholinium-3 and this results in reduced synthesis of ACh (1–3). Under some circumstances ACh metabolism in the brain appears to be affected by parenteral (4) or dietary (5, 14) administration of Ch. The production of AcCoA can apparently be reduced by inhibition of the utilization of pyruvate or glucose, which also decreases the synthesis of ACh (6, 7). Recent experiments by Barker and Mittag (8, 9) led them to propose that the high affinity transport of Ch and the subsequent transfer of an acetyl group from AcCoA, catalyzed by Ch acetyltransferase (CAT), were directly coupled. We have tested this hypothesis by reducing the availability of AcCoA and measuring both the rate of transport of Ch by the high affinity system and the rate at which it is converted to ACh
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Choline and phospholipid metabolism and the synthesis of acetylcholine in rat brain
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The Utilization of Choline and Acetyl Coenzyme A for the Synthesis of Acetylcholine
Acetylcholine synthesis in rat brain synaptosomes was investigated with regard to the intracellular sources of its two precursors, acetyl coenzyme A and choline. Investigations with α‐cyano‐4‐hydroxycinnamate, an inhibitor of mitochondrial pyruvate transport, indicated that pyruvate must be utilized by pyruvate dehydrogenase located in the mitochondria, rather than in the cytoplasm, as recently proposed. Evidence for a small, intracellular pool of choline available for acetylcholine synthesis was obtained under three experimental conditions. (1) Bromopyruvate competitively inhibited high‐affinity choline transport, perhaps because of accumulation of intracellular choline which was not acetylated when acetyl coenzyme A production was blocked. (2) Choline that was accumulated under high‐affinity transport conditions while acetyl coenzyme A production was impaired was subsequently acetylated when acetyl coenzyme A production was resumed. (3) Newly synthesized acetylcholine had a lower specific activity than that of choline in the medium. These results indicate that the acetyl coenzyme A that is used for the synthesis of acetylcholine is derived from mitochondrial pyruvate dehydrogenase and that there is a small pool of choline within cholinergic nerve endings available for acetylcholine synthesis, supporting the proposal that the high‐affinity transport and acetylation of choline are kinetically coupled
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