EFFECTS OF EXCITATION-BLOCKING DRUGS AND SODIUM DEFICIENCY ON THE VERATRINE ELECTRICAL RESPONSE

¹ Department of Biology, Washington Square College of Arts and Science, New York University , New York

Effects on the veratrine response of the curarized frog sartorius muscle were determined in the presence of whole-muscle treatment with non-blocking concenitrations of eserine, DFP, and procaine, and 80 per cent deficiency in external Na concentration. Using direct coupled amplification, the electrical features were recorded by an external electrode at a muscle spot locally treated with veratrine. Mechanical changes were recorded isotonically after whole-muscle exposure to veratrine.

Eserine, DFP, and procaine all antagonized the veratrine response in a generally similar manner: a) by reducing the duration of the initial period of electrical repetitive firing and of the associated mechanical tetanus, and b) by curtailing the later depolarization and associated mechanical contracture.

Prostigmine did not alter the veratrine response in any way.

A primary effect of the Na deficiency was to suppress, completely or almost completely, the tetanus phase, both electrical and mechanical, of the veratrine output. A secondary effect, sometimes observed, was curtailment of the depolarization and the mechanical change of the contracture phase.

The consistency of the electromechanical correlations under the various conditions of the experiments demonstrated that veratrine and its antagonists act only on the muscle fiber membrane, and that the contractile behavior in each case is an indirect consequence of the changes in membrane electrical state.

The fact that only the penetrating drugs, or transmembrane change (Na deficiency), antagonized veratrine indicates that the locus of both veratrine action and its antagonism is within the membrane or at its inner surface.

The results suggest that a) eserine, DFP, and procaine exert their antagonistic effects by actions on some component, not necessarily the same for all these drugs, of the antiacetylcholinesterase system, b) procaine may affect the role of K in veratrine action, and c) the Na deficiency effects are due to arm increase in resting membrane potential.