Effects of acetylcholine on axonal conduction of lobster nerve.

Abstract

Acetylcholine and related compounds have been tested for their effects on the electrical activity of lobster walking-leg nerve bundles. Changes in action and membrane potential were recorded with the “sucrose-gap” technique. ACh in concentrations of 5·10−3–10−2 M decreases the membrane potential; the simultaneously recorded action potentials initially display an increased amplitude and a marked prolongation and elevation of the descending phase which appears oscillatory. As the depolarization progresses, the spike height decreases and the effects on the descending phase decline. Finally reversible block of conduction occurs. d,l-Acetyl-β-methylcholine (10−2 M) produces similar effects on the action potential but the membrane potential is only slightly depolarized. Choline, acetate and bromide in concentrations equal to those of ACh have no effect; in 10-fold higher concentrations only choline produces minor changes in the action potential. Physostigmine (5 mM) produces effects similar to those seen with ACh while lower concentrations inhibit the action of ACh. Atropine and tetracaine reversibly block conduction and like physostigmine, also inhibit the effect of ACh. Although curare was nerve demonstrated to block conduction, it does inhibit the action of ACh. Irreversible cholinesterase inhibitors (phospholine, Paraoxon) block conduction. Paraoxon much faster than phospholine. The membrane potential is decreased by 20–30 mV, and while the effects of these inhibitors on the membrane potential are reversible, conduction remains blocked. The difficulties of interpreting some of these actions on a nerve bundle are discussed.