Evidence for the regulatory function of synaptoplasmic acetyl-CoA in acetylcholine synthesis in nerve endings.
Isolated synaptosomes maintained a relatively stable level of acetyl-CoA during their incubation in the presence of 30 mM-KCl. Addition of Ca2+ resulted in inhibition of pyruvate oxidation and slight activation of acetylcholine synthesis. The cation decreased acetyl-CoA in intrasynaptosomal mitochondria, but did not alter its content in synaptoplasm. Verapamil did not affect pyruvate oxidation, but decreased acetyl-CoA in synaptoplasm and inhibited acetylcholine synthesis in synaptosomes. It indicates that Ca2+ might regulate acetylcholine synthesis through changes in the direct transfer of acetyl-CoA from mitochondria to synaptoplasm.
Bielarczyk
H
H
Department of Clinical Biochemistry, Medical Academy, Gdańsk, Poland.
Szutowicz
A
A
D000105:Acetyl Coenzyme A / Q000378:metabolism*; D000109:Acetylcholine / Q000096:biosynthesis*; D000818:Animals; D001921:Brain / Q000201:enzymology; D002118:Calcium / Q000378:metabolism; D004072:Digitonin / Q000494:pharmacology; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D009411:Nerve Endings / Q000187:drug effects / Q000201:enzymology*; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013574:Synaptosomes / Q000201:enzymology; D014700:Verapamil / Q000494:pharmacology
D011773:Pyruvates; D000105:Acetyl Coenzyme A; D014700:Verapamil; D004072:Digitonin; D000109:Acetylcholine; D002118:Calcium