ABSTRACT
The compound action potential recorded from the pleural-supraintestinal connective of Viviparus contectus consists of a large, slow component with an average conduction velocity of about 0·02 m/sec (at 23 °C) and a faster component with a conduction velocity of 0·10 m/sec (at 23 °C) for the fastest fibres.
Both fast and slow action potentials are rapidly abolished by the substitution of tris chloride and choline chloride for the sodium salts of normal Ringer. Tetrodotoxin, applied at 10−5 M rapidly abolishes action potentials in all fibres. It is, therefore, concluded that a largely sodium-dependent mechanism of spike generation operates in all axons of the connective.
Lithium ions effectively substitute for sodium ions in maintaining the fast action potentials for extended periods, whereas tetraethylammonium ions do not.
When the calcium chloride of normal Ringer is replaced by sucrose, magnesium chloride or barium chloride, conduction of fast action potentials is maintained. A small increase in the sensitivity of all axons to tetrodotoxin is observed in calcium-free Ringer ; a slight reduction in the spike amplitude of fast action potentials follows the application of manganous ions at 5 mM/1 in normal Ringer. It is concluded that any possible contribution of calcium to the generation of the action current of the fast action potential is very small compared to that of sodium.
All axons of the connective function for extended periods in sodium-free (dextran) Ringer. Under these conditions, tetrodotoxin blocks conduction in all fibres at concentrations of 10−6 M, suggesting that function in dextran Ringer is maintained by a sodium-dependent mechanism.
Relative conduction velocity (θtest/θnormal) of a given component of the compound action potential is the ratio of the conduction velocity obtained in the test solution to that obtained in normal Ringer.
