Abstract
Stretching of the muscle spindle produces a receptor potential (a local depolarization) in the muscle spindle which gives rise to repetitive spikes in the sensory nerve (1). In addition, it has been suggested that the dynamic component of the receptor potential is simply the result of a change in membrane capacity, and that the successive static component may be due to a change in membrane permeability (1).
Henatsch and Schulte (2) found that the afferent discharges from the muscle spindle were increased by acetylcholine or succinylcholine in the muscle of frog. Ottoson (3) reported that acetylcholine (1×10-4 g/ml) had no significant effect on the sensory endings while higher concentrations caused a slight reduction of their activity. Some reports (4-6) indicated that d-tubocurarine or atropine affected the discharges from the muscle spindle. The problem thus remains whether acetylcholine or cholinesters play an essential role in the generation or transmission of spikes.
It was expected that use of various anticholinergics might provide an important clue in elucidating the mechanism of static generation and transmission of spikes. Strychnine was shown to have curare-like action (7) and also depressive action on the afferent discharges from the muscle spindle (8). The present study deals with d-tubocurarine, atropine, hexamethonium, hemicholinium-3, procaine and also strychnine. It is concerned with effects on muscle spindle discharges, receptor potential, nerve conduction and muscle twitch.
