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POSTSYNAPTIC EFFECTS OF SOME CENTRAL STIMULANTS AT THE NEUROMUSCULAR JUNCTION
Author(s) -
GAGE PETER W.,
SAH PANKAJ
Publication year - 1982
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.1476-5381.1982.tb09166.x
Subject(s) - chemistry , time constant , postsynaptic potential , neuromuscular transmission , amplitude , neuromuscular junction , biophysics , extracellular , sartorius muscle , acetylcholine , exponential decay , acetylcholinesterase , anesthesia , neuroscience , pharmacology , physics , biochemistry , enzyme , medicine , receptor , nuclear physics , electrical engineering , biology , engineering , quantum mechanics
1 Miniature endplate currents (m.e.p.cs) were recorded with extracellular electrodes from sartorius muscles of toads. 2 Central excitant analogues of amylobarbitone (3M2B) and halothane (DBE) decreased the amplitude and time constant of decay of m.e.p.cs and hence reduced the amplitude of miniature endplate potentials. The decay remained exponential with single time constant. 3 A central excitant analogue of ether (indoklon) reduced the amplitude of m.e.p.cs and made their decay biphasic. The decay could be fitted by the sum of two exponentials. 4 Bemegride, a central excitant, prolonged m.e.p.cs. Their decay remained exponential with single time constant. The effect was not due to inhibition of acetylcholinesterase. 5 All of the drugs tested, including amylobarbitone, reduced the temperature‐sensitivity of the decay of m.e.p.cs. 6 The biphasic decay of m.e.p.cs caused by indoklon could not be explained simply by supposing that the drug blocked open endplate channels unless it was assumed that the normal rate of channel closing also increased and became much less temperature‐sensitive than normal.