Origin of axon membrane hyperpolarization under sucrose-gap.

One of the disadvantages of the sucrose-gap method for measuring membrane potentials with extracellular electrodes is a membrane hyperpolarization of the order of 30 to 60 mv, as compared with the resting potential obtained with intracellular microelectrodes in the absence of a sucrose-gap. In the present study the contribution of the sucrose-sea water junction potential to this hyperpolarization effect has been evaluated by comparing the effects on the resting potential of several anion and cation substitutions in the sea water bathing the lobster giant axon under sucrose-gap. Measurements with microelectrodes demonstrate a significant liquid junction potential between sucrose and standard artificial sea water. The value of this liquid junction potential as well as the measured resting membrane potential varies as a function of the anions and cations substituted in the sea water. Both the liquid junction potential and the sucrose-gap-induced hyperpolarization can be eliminated by using a low mobility anion to replace most of the chloride in sea water while the normal cation content remains unchanged. These data provide evidence that loop currents at the sucrose-sea water-axon junctions are at least partly responsible for membrane hyperpolarization under a sucrose gap.