Fariñas I, Solsona C, Marsal J
Departament de Biologia Cellular i Anatomia Patològica, Facultat de Medicina, Hospital de Bellvitge, Universitat de Bärcelona, Spain.
Neuroscience. 1992;47(3):641-8. doi: 10.1016/0306-4522(92)90172-x.
We have examined the effect of several blockers of voltage-sensitive calcium channels on the release of acetylcholine and ATP from synaptosomes isolated from Torpedo marmorata electric organ. Depolarization of these nerve terminals with high K(+)-containing solutions resulted in a calcium-dependent release of both molecules. Cadmium ions (10(-6) to 10(-3) M) inhibited similarly both releases whereas nickel ions (10(-4) M) in the external medium did not affect either neurotransmitter or nucleotide release. Both releases were completely resistant to the effect of 1,4-dihydropyridines (antagonists nimodipine, nifedipine and agonist Bay K 8644) and of a related compound (diltiazem) at concentrations up to 10(-5) M. These drugs failed to cause any effect even when synaptosomes were submaximally depolarized during incubation. Omega-conotoxin (10(-8) to 5 x 10(-5) M) showed a differential effect on acetylcholine and ATP releases. Nucleotide release was inhibited 90% at the highest concentration tested (50 microns) while acetylcholine release was only moderately decreased (30%). EC50 values for acetylcholine and ATP were of 167 and 2 microM respectively. The results suggest the implication of different types of calcium channels in the release of these molecules.
