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Tacrine‐induced increase in the release of spontaneous high quantal content events in Torpedo electric organ
Author(s) -
Cantí Carles,
Martí Eulàlia,
Marsal Jordi,
Solsona Carles
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb13022.x
Subject(s) - tacrine , physostigmine , torpedo , cholinesterase , cholinergic , chemistry , acetylcholinesterase , free nerve ending , pharmacology , biophysics , medicine , biochemistry , biology , acetylcholine receptor , enzyme , receptor
1 The anticholinesterases, tacrine (100 μ m ) and physostigmine (60 μ m ) 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.