Biochemical evidence that acetylcholine release from cholinergic nerve terminals is mostly vesicular.
The nature of the intraterminal compartments from which acetylcholine (ACh) is released following presynaptic stimulation was investigated. This was pursued by examining the effects of the anticholinergic drug 2-(4-phenylpiperidino)cyclohexanol (AH5183) on the release of newly synthesized [3H]ACh and of endogenous ACh from purified cholinergic nerve terminals (synaptosomes) which were isolated from the electric organs of Torpedo. Preincubation of the synaptosomes, with AH5183 (1-10 microM), does not affect either the intraterminal synthesis of [3H]ACh or the uptake of its precursors, but results in a marked inhibition (85%) of the release of the newly synthesized [3H]ACh. However, when AH5183 is added following the accumulation of [3H]ACh in the nerve terminals, it does not affect [3H]ACh release. AH5183 also has no effect on the release of preformed endogenous ACh. These findings, together with the previous in vitro demonstrations that AH5183 is a potent inhibitor of ACh uptake into isolated cholinergic vesicles, suggest that most of the synaptosomal ACh is secreted by a vesicular mechanism.
D000085:Acetates / Q000378:metabolism; D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D004557:Electric Organ / Q000378:metabolism; D066298:In Vitro Techniques; D010622:Phencyclidine / Q000031:analogs & derivatives / Q000494:pharmacology; D010880:Piperidines; D013572:Synaptic Vesicles / Q000378:metabolism* / Q000648:ultrastructure; D013574:Synaptosomes / Q000378:metabolism; D014101:Torpedo
D000085:Acetates; D010880:Piperidines; C006189:vesamicol; D010622:Phencyclidine; D000109:Acetylcholine