Tacrine‐induced increase in the release of spontaneous high quantal content events in Torpedo electric organ

• Published in: British journal of pharmacology Vol. 112; no. 1; pp. 19 - 22
• Main Authors: Cantí, Carles, Martí, Eulàlia, Marsal, Jordi, Solsona, Carles
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.1994; Nature Publishing
• Subjects: acetylcholine; Acetylcholine - metabolism; acetylcholinesterase; Alzheimer's disease; Animals; apyrase; Biological and medical sciences; Cholinesterase Inhibitors - pharmacology; Electric Organ - drug effects; Electric Organ - enzymology; Electric Organ - metabolism; Electrophysiology; In Vitro Techniques; Kinetics; Medical sciences; Membrane Potentials - drug effects; Microelectrodes; miniature endplate currents; Miscellaneous; Motor Endplate - drug effects; Nerve Endings - drug effects; Nerve Endings - enzymology; Neuropharmacology; Pharmacology. Drug treatments; physostigmine; Physostigmine - pharmacology; quantal transmitter release; Synaptosomes - drug effects; Synaptosomes - enzymology; Synaptosomes - metabolism; Tacrine; Tacrine - pharmacology; Torpedo; Torpedo - physiology; Torpedo marmorata; Vertebrata; Alzheimer disease; Pisces; Torpedo marmorata; Electrophysiology; Electric organ; Acetylcholine; Anticholinesterase agent; Mechanism of action; In vitro; Biological activity; Cholinergic transmission
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1994.tb13022.x

1 The anticholinesterases, tacrine (100 μm) and physostigmine (60 μm) had different effects on the amplitude distribution and kinetics of miniature endplate currents (m.e.p.cs) recorded extracellularly from the electric organ of Torpedo marmorata. 2 Tacrine increased the ratio of giant miniatures (larger than 4 mV of amplitude) to more than 20% of recorded spontaneous events. In the presence of physostigmine such events represented only 4%. 3 Both tacrine and physostigmine increased the rise time and the decay phase of normal‐sized m.e.p.cs when compared to control conditions. Both effects were significantly greater for tacrine. 4 We have tested the specificity of the tacrine effect on ectoenzyme activities associated with plasma membranes of these pure cholinergic nerve endings. Tacrine does not act unspecifically on every ectoenzyme, because it is not able to block the ectoapyrase activity even at a concentration 100 fold greater than that required to inhibit 94% of AChE. 5 We conclude that the differential effects of tacrine and physostigmine can be explained in terms of undetermined presynaptic actions of tacrine, while comparable effects of the two compounds can be explained through a shared anticholinesterase activity.