Vesicular storage and release of a false cholinergic transmitter (acetylpyrrolcholine) in the Torpedo electric organ

Abstract

The choline analogue N-[Me- 3H] N-hydroxyethyl-pyrrolidinium (pyrrolcholine) was studied in the Torpedo electric organ. Pyrrolcholine is transported into isolated nerve terminal sacs by the choline high affinity uptake system ( K T = 5.7 μ m). If blocks of electric tissue are perfused in the presence of both [ 3H]pyrrolcholine and [ 14C]choline both compounds become acetylated and are taken up into synaptic vesicles. This process is enhanced by low frequency stimulation (~0.1 Hz). Upon subsequent stimulation of the nerve at 5 Hz both acetylpyrrolcholine and acetylcholine are released into the perfusate by a calcium-sensitive mechanism; their molar ratio in the perfusate is the same as that for their loss from the vesicle fraction. Acetylpyrrolcholine is a potent agonist on the frog rectus abdominis muscle although 12.7-fold less active than acetylcholine. We conclude that pyrrolcholine is a precursor of a cholinergic false transmitter in the Torpedo electric organ. Acetylpyrrolcholine has been shown to fulfil all the criteria for the definition of a false transmitter, including storage in synaptic vesicles.