Adenosine and related nucleotides alter calcium uptake in depolarized synaptosomes of torpedo electric organ.

Calcium has been shown to enter cholinergic synaptosomes transiently during potassium-induced depolarization, in which ACh and ATP are released together. Because junctional ATP is rapidly hydrolyzed by extracellular ATPases, I studied and compared the roles of ATP, ADP, AMP, and adenosine (Ade) on the control of calcium uptake during depolarization. Pure cholinergic synaptosomes of Torpedo fish electric organ were depolarized by high potassium concentrations and the amount of calcium uptake was then measured in the presence of equal concentrations of Ade and its related nucleotides. Calcium uptake was more inhibited when the nucleotide was less phosphorylated. Thus, Ade was the greatest inhibitor. Because Ade is quickly and actively taken up from the extracellular medium by synaptosomes and converted intracellularly to ATP, I also measured the capacity of Ade, after its initial inhibitory action, to reactivate the calcium uptake. After a short preincubation with Ade, the later uptake of calcium was enhanced. The combined results support a complete role of adenosine and related nucleotides in the control of calcium movement across the presynaptic membrane.