» Articles » PMID: 3501570

The Effect of Anticholinesterase Drugs on the Ionophoretically-evoked End-plate Currents

Overview
Journal Pflugers Arch
Specialty Physiology
Date 1987 Nov 1
PMID 3501570
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

In order to study the sensitivity of acetylcholine (ACh) receptors exposed to anticholinesterase drugs, the ionophoretically evoked end-plate currents (e.p.c.i) in frog sartorius muscle were studied. During treatment with prostigmine (PST, 3 microM) or methanesulfonyl fluoride (MSF, 1-2 mM), the amplitude of the e.p.c.i evoked by ACh was first increased, reaching its maximum (200-400%) after 20-30 min and then decreased. If these experiments were repeated by applying carbachol (CCh) instead of ACh, an increase, although less pronounced (30-100%), was also observed. The results obtained by applying CCh cannot be ascribed to the inhibition of ACh-esterase, as CCh is not hydrolysed by this enzyme. Therefore, a direct action of both drugs on the ACh-receptor channel complex is suggested. From the comparison of the effects of PST and MSF on the responses to CCh and ACh applications, it is calculated that 20-25% of the increased response to ACh during PST treatment can be ascribed to the direct effect on the ACh-receptor channel complex. During MSF treatment, this amount results in 13-15%. The changes of the time course of the e.p.c.i (evoked by CCh or ACh), which is prolonged in the presence of PST and shortened during the maximum effect of MSF, suggest that the direct action of both studied drugs is different.

Citing Articles

Effects of irreversible and reversible cholinesterase inhibitors on single acetylcholine-activated channels.

Zorec R, Scuka M, Kordas M J Membr Biol. 1992; 125(1):41-8.

PMID: 1371811 DOI: 10.1007/BF00235796.

References
1.
Akaike A, Ikeda S, Brookes N, Pascuzzo G, Rickett D, Albuquerque E . The nature of the interactions of pyridostigmine with the nicotinic acetylcholine receptor-ionic channel complex. II. Patch clamp studies. Mol Pharmacol. 1984; 25(1):102-12. View

2.
White R, Gardner D . Physostigmine prolongs the elementary event underlying decay of inhibitory postsynaptic currents in Aplysia. J Neurosci. 1983; 3(12):2607-13. PMC: 6564667. View

3.
Kordas M, Brzin M, Majcen Z . A comparison of the effect of cholinesterase inhibitors on end-plate current and on cholinesterase activity in frog muscle. Neuropharmacology. 1975; 14(11):791-800. DOI: 10.1016/0028-3908(75)90106-9. View

4.
Gage P, McBurney R . Effects of membrane potential, temperature and neostigmine on the conductance change caused by a quantum or acetylcholine at the toad neuromuscular junction. J Physiol. 1975; 244(2):385-407. PMC: 1330769. DOI: 10.1113/jphysiol.1975.sp010805. View

5.
McMahan U, Sanes J, Marshall L . Cholinesterase is associated with the basal lamina at the neuromuscular junction. Nature. 1978; 271(5641):172-4. DOI: 10.1038/271172a0. View