Choline uptake and metabolism in affinity-purified cholinergic nerve terminals from rat brain.
Cholinergic nerve terminals were affinity purified from rat caudate nucleus. These terminals possessed both high- (KT = 2.7 microM) and low- (KT = 58 microM) affinity uptake mechanisms for exogenous [3H]choline. The proportion of [3H]choline acetylated was reduced from 75 to 30% under conditions of anoxia and hypoglycaemia, whereas the phosphorylation of choline increased from 4 to 52%. Choline phosphorylation was also increased when the terminals were preloaded with choline. The affinity-purified terminals were shown to release acetylcholine in a Ca2+-dependent manner on depolarization. The relationship between choline acetylation and phosphorylation in the cholinergic nerve terminal is discussed.
D000107:Acetylation; D000109:Acetylcholine / Q000096:biosynthesis; D000818:Animals; D002421:Caudate Nucleus / Q000378:metabolism*; D002794:Choline / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D006426:Hemicholinium 3 / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D010100:Oxygen / Q000494:pharmacology; D010766:Phosphorylation; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000494:pharmacology
D006426:Hemicholinium 3; D012964:Sodium; D005947:Glucose; D002794:Choline; D000109:Acetylcholine; D010100:Oxygen