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Effects of tetraethylammonium chloride on sympathetic neuromuscular transmission in saphenous artery of young rabbits.
Author(s) -
Holman M E,
Surprenant A
Publication year - 1980
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1980.sp013375
Subject(s) - tetraethylammonium chloride , tetraethylammonium , excitatory postsynaptic potential , chemistry , depolarization , membrane potential , resting potential , biophysics , anatomy , neuromuscular junction , anesthesia , medicine , inhibitory postsynaptic potential , potassium , neuroscience , biology , biochemistry , organic chemistry
1. Excitatory junction potentials and electrotonic potentials were recorded from the smooth muscle of the rabbit saphenous artery using intracellular electrodes. 2. Tetraethylammonium chloride (TEA) in concentrations greater than 3.5 mM caused depolarization. Concentrations greater than 5 mM caused spontaneous electrical activity in the form of excitatory junction potentials (e.j.p.s) and all‐or‐nothing action potentials which were associated with spontaneous mechanical activity. 3. Concentrations of TEA less than 2.5 mM did not alter the resting potential nor the passive membrane properties of the smooth muscle over a range of +/‐ 15 mV. 4. The following effects were observed in 2.0 mM‐TEA. (a) The minimum stimulus strength required for the initiation of an e.j.p. fell by three to fivefold. (b) Single stimuli that elicited only a small e.j.p. in normal solution evoked an all‐or‐nothing action potential of up to 70 mV amplitude. (c) Whereas in normal solution e.j.p.s could only be recorded up to 7 mm away from the perivascular stimulating electrode e.j.p.s could be recorded at distances of up to 13 mm. (d) The duration of the e.j.p. was prolonged. 5. Based on these results and the effects of TEA reported for other synapses it is proposed that TEA may act to increase the amount of transmitter released per axon, to increase the duration of release and to cause an increased invasion throughout the autonomic ground plexus by nerve impulses. This would imply that in normal solution, in vitro, the action potential may not propagate throughout the whole length of the terminal axon and its many branches due to failure of conduction at one or more points along the terminal portion of the axon.