1. Acetylcholine (ACh), 7.5 x 10(-5) M, and carbachol, 5 x 10(-6) M (CCh) depressed the frequency of miniature endplate potentials (m.e.p.ps) in the frog (Rana temporaria) sartorius neuromuscular junction with active acetylcholinesterase to about 50-55% of the controls. 2. A similar depression was produced by the nicotinic agonists, nicotine, suberyldicholine and tetramethylammonium. 3. The muscarinic agonists, oxotremorine, methylfurmethide and methacholine were without effect on m.e.p.p. frequency. The muscarinic antagonist, atropine and the nicotinic antagonist, (+)-tubocurarine, had no effect on the depression of m.e.p.p. frequency evoked by CCh. 4. The ganglionic blockers, benzhexonium and IEM-1119, were also without effect on the CCh-evoked depression of m.e.p.p. frequency. 5. Pretreatment of muscles with anticholinesterases did not prevent the CCh-induced drop in m.e.p.p. frequency. 6. The effect of CCh was proportionally the same as in the controls in preparations where the m.e.p.p. frequency was changed by elevation of K+ and in the presence of theophylline, noradrenaline, dibutyryl adenosine 3':5'-cyclic monophosphate (db cyclic AMP) and db cyclic GMP. 7. An inhibitor of Na+,K(+)-ATPase, ouabain, 5 x 10(-5) mol l-1, prevented or reversed the depression of m.e.p.p. frequency by CCh. However, the depression was present in a nominally K(+)-free medium. Insulin and adrenaline, which are considered to be Na+,K(+)-ATPase activators, were without effect on depression of m.e.p.p. frequency. 8. The depression of m.e.p.p. frequency by 5 x 10(-6) M CCh was the same at temperatures between 5 and 30 degrees C with a Q10 near to 1.0. When threshold amounts of CCh were used (6 x 10-7 and 3 x 10-7 M), the depression was less at higher temperatures.9. The receptive structures responsible for the CCh (or ACh)-evoked depression of m.e.p.p. frequency differ pharmacologically from muscarinic, nicotinic ganglionic and neuromuscular junction ACh-receptors as well as from the synaptic cholinesterase, in contrast to previous reports (Duncan & Publicover, 1979).The low temperature-dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics.

Institute of Physiology Czechoslovak Academy of Sciences Prague

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Pflugers Arch. 1987 Jul;409(3):258-64 PubMed

Pharmacol Rev. 1966 Mar;18(1):145-61 PubMed

J Cell Biol. 1985 Nov;101(5 Pt 1):1953-65 PubMed

Pharmacol Rev. 1985 Mar;37(1):81-132 PubMed

J Physiol. 1990 Apr;423:631-40 PubMed

J Gen Physiol. 1981 Sep;78(3):313-44 PubMed

Brain Res. 1983 Mar 28;264(1):89-97 PubMed

Pflugers Arch. 1981 Sep;391(3):213-8 PubMed

Biochim Biophys Acta. 1982 Dec 22;693(2):273-9 PubMed

Naunyn Schmiedebergs Arch Pharmacol. 1981 Apr;316(2):131-4 PubMed

J Physiol. 1979 Sep;294:91-103 PubMed

J Physiol. 1979 Jan;286:1-14 PubMed

J Physiol. 1977 Oct;271(3):817-46 PubMed

J Physiol. 1977 Oct;271(3):605-24 PubMed

Farmakol Toksikol. 1955 Mar-Apr;18(2):21-7 PubMed

J Physiol. 1952 May;117(1):109-28 PubMed

J Physiol. 1956 Jun 28;132(3):650-66 PubMed

J Physiol. 1963 Nov;169:431-7 PubMed

J Pharmacol Exp Ther. 1963 Oct;142:21-3 PubMed

Nature. 1962 Mar 10;193:986-7 PubMed

Biochim Biophys Acta. 1958 Dec;30(3):653-4 PubMed

J Physiol. 1988 Sep;403:135-49 PubMed

Int Rev Neurobiol. 1985;27:299-336 PubMed

Neirofiziologiia. 1986;18(5):586-93 PubMed

Physiol Rev. 1986 Jul;66(3):542-80 PubMed

J Membr Biol. 1986;91(2):165-72 PubMed

J Physiol. 1976 Sep;260(3):687-717 PubMed

Prog Neurobiol. 1979;12(3-4):181-290 PubMed

Neuroscience. 1978;3(4-5):367-84 PubMed

Dokl Akad Nauk SSSR. 1979;249(6):1488-91 PubMed

Prog Brain Res. 1979;49:183-9 PubMed

Pflugers Arch. 1979 May 15;380(1):101-4 PubMed

Pflugers Arch. 1977 Sep 16;370(3):295-7 PubMed

Life Sci. 1977 Jun 1;20(11):1839-45 PubMed

Proc Natl Acad Sci U S A. 1979 Dec;76(12):6336-40 PubMed

Biull Eksp Biol Med. 1979 Feb;87(2):171-4 PubMed

J Physiol. 1973 Dec;235(3):655-91 PubMed

J Physiol. 1970 Dec;211(3):551-70 PubMed

J Physiol. 1965 Dec;181(3):487-97 PubMed

Science. 1971 Jun 4;172(3987):1034-6 PubMed

J Physiol. 1975 May;247(1):209-26 PubMed

Proc Natl Acad Sci U S A. 1974 Apr;71(4):1489-92 PubMed

Proc Natl Acad Sci U S A. 1969 Sep;64(1):134-41 PubMed

J Neurocytol. 1974 Mar;3(1):109-31 PubMed

Mol Pharmacol. 1986 Dec;30(6):631-8 PubMed

From Frog Muscle to Brain Neurons: Joys and Sorrows in Neuroscience

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