Cytoplasmic pH (pH1) of crayfish lateral giant axons was monitored using antimony microelectrodes placed near septate junctions and variations of internal pH was induced by short applications of ammonium sulfate in the perfusing bath of the preparation. This treatment produced a rapid cell alkalinization followed, after wash, by acidification rebound. Simultaneously, two successive phases of uncoupling of the septate junction occurred; they had the same time course as those of their associated pH1 movements. Calculation of the electronic coupling parameters indicated that, during alkalinization, coupling was accompanied by an increased axonal membrane conductance (the intimate origin of which was beyond the scope of this study) and resulted from a shunt of the gap junctions; the resistance proper of the latter was unaffected; thus involvement of Ca2+ was ruled out and uncoupling was only an indirect consequence of the electrotonic junction's network configuration. In contrast, and as expected from previous investigations, the junctional membrane resistance was increased during the second phase of cytoplasmic acidification. Evidence that uncoupling can be brought about by a non-junctional membrane increased permeability raises questions about some of the criteria commonly used during investigations of electrotonic transmission.