Possible involvement of endogenous acetylcholine in the tetraethylammonium induced depolarization of avian skeletal muscle.

The depolarization produced by acetylcholine (ACh) (5.5 microM-11 mM) and by tetraethylammonium (TEA) (0.95-48 mM) in chick skeletal muscle were recorded using a sucrose-gap external recording device. The gap is constructed from perspex blocks of 3 main chambers which contain the preparation and are superfused with Krebs solution (chamber 1), Krebs solution containing test drug solution (chamber 3) and isotonic sucrose solution (chamber 2). Drugs were added directly into the superfusion stream leading to chamber 3 which contained the distal and active part of the muscle. Recordings of electrical responses were made via a pair of calomel electrodes, in contact with woollen wicks extending from chambers 1 and 3, leading to a preamplifier linked to a cathode ray oscilloscope and a potentiometric pen recorder. The results showed that TEA, a potassium channel blocker, produced a small depolarization (about 1 mV), whereas ACh produced a large depolarization (about 8 mV), and that the TEA-induced depolarization was in part due to the release of endogenous ACh at the neuromuscular junction. Other findings include the characteristic feature of TEA-induced depolarization, i.e. its long latency (about 1 min) and the biphasic response, a small depolarization followed by an after-hyperpolarization (about 2 mV). The results are in favour of the possibility that TEA may act at both pre- and postsynaptic membranes at the avian neuromuscular junction.