Salgado_1996_Neurosci.Lett_204_37

The aim of the present experiments was to test whether vesamicol alters the evoked release of ATP from nerve terminals. Continuous or cumulative release of ATP evoked by 33 mM KC1 from rat cerebrocortical synaptosomes was largely calcium-dependent. Vesamicol interfered with release of ATP from synaptosomes depolarized with KCl (33 mM) in a dose-dependent and stereoselective way. The (-)-vesamicol decreased the output of ATP in doses much lower than (+)-vesamicol. The release of the major excitatory neurotransmitter glutamate from depolarized nerve endings was not impaired by vesamicol. We suggest that vesamicol may alter the release of ATP specifically, probably by interacting with a protein similar to the vesamicol receptor found in cholinergic synaptic vesicles.