Anesthetic blocking of nerve membrane conductances by internal and external applications

Abstract

Dibucaine hydrochloride, pentobarbital sodium, tropine p‐tolyl acetate hydrochloride (tertiary form), and tropine p‐tolyl acetate methiodide (quaternary form) reversibly blocked both peak transient and steadystate components of conductance changes from either side of the squid nerve membrane. With external and internal applications of dibucaine and with internal application of the tertiary topine, the steady‐state current declined somewhat, leaving a “hump.” The time to the early peak transient current was unaffected by either external or internal application of dibucaine, but prolonged by either external or internal application of pentobarbital. The curve relating the peak transient conductance to the membrane potential was shifted along the potential axis in the direction of depolarization by external or internal application of pentobarbital. It is suggested that the mechanism of blockage of the peak transient conductance by these anesthetic agents is different from that by tetrodotoxin or by uncharged lipid‐soluble chemicals.