mr-16728 and cetiedil

mr-16728 has been researched along with cetiedil* in 2 studies

Other Studies

2 other study(ies) available for mr-16728 and cetiedil

ArticleYear
Cyclosporin A affects functions concerning acetylcholine release of cholinergic Torpedo synaptosomes.
    European journal of pharmacology, 1996, Feb-05, Volume: 296, Issue:3

    The effect of cyclosporin A was investigated on Torpedo synaptosomes. Cyclosporin A inhibits KCl-evoked acetylcholine release (up to 50% at 1 mu M) and was inactive on acetylcholine release induced by a Ca2+ ionophore, A23187. Interestingly, when the synaptosomes were pretreated with cyclosporin A, this immunosuppressor did abolish the modulation of A23187-induced acetylcholine release produced by two other drugs, cetiedil (alpha-cyclohexyl-3-thienyl acetic acid 2-(hexahydro-1H-azepin-1-yl) ethyl ester, citrate salt) and MR16728 (N-(N'-hexamethylene imino)-propyl-phenyl-cyclohexyl-methyl acetamide, chlorhydrate), which were previously shown to be inhibitory and stimulatory, respectively. Moreover, cyclosporin A and MR16728 are competitive inhibitors of [3H]cetiedil binding to purified synaptosomal presynaptic membranes (dissociation constant of 181.9 nM). These results suggest that presynaptic proteins involved in acetylcholine release (directly or indirectly through cyclophilin) are potential targets of cyclosporin A in Torpedo synaptosomes.

    Topics: Acetamides; Acetanilides; Acetylcholine; Animals; Azepines; Calcimycin; Calcium; Cyclosporine; Immunosuppressive Agents; Potassium Chloride; Synaptosomes; Torpedo

1996
Spontaneous release of acetylcholine from Torpedo synaptosomes: effect of cetiedil and its analogue MR 16728.
    Journal of neurochemistry, 1994, Volume: 62, Issue:1

    The effects of cetiedil and its analogue MR 16728 were examined on spontaneous acetylcholine release measured with a chemiluminescent assay using choline oxidase in a synaptosomal suspension obtained from Torpedo marmorata electric organ. Evoked acetylcholine release is inhibited by cetiedil, whereas this drug enhances spontaneous extracellular Ca(2+)-independent acetylcholine release (up to 340%). This effect was examined as a function of cetiedil concentration and incubation time. On the other hand, the analogue MR 16728, which enhances A23187-evoked acetylcholine release, also enhances spontaneous Ca(2+)-independent acetylcholine release. Cetiedil and MR 16728 effects on spontaneous acetylcholine release were also examined in the presence of Ca2+. Addition of Ca2+ enhanced spontaneous acetylcholine release by 75%, and cetiedil and MR 16728 stimulation was maintained but with different levels of enhancement. Thus, these results show that the processes responsible for evoked and spontaneous acetylcholine release are sensitive but in different ways to drugs of the cetiedil family.

    Topics: Acetamides; Acetanilides; Acetylcholine; Animals; Anti-Arrhythmia Agents; Azepines; Calcimycin; Calcium; Electric Organ; Kinetics; Parasympathomimetics; Synaptosomes; Time Factors; Torpedo

1994