Role of electrogenic sodium pump in slow synaptic inhibition is re-evaluated

Abstract

THE mechanism of synaptic transmission at most synapses involves an increase in conductance of the postsynaptic membrane to certain ions^1,2. Certain slow postsynaptic inhibitions in both the central and peripheral nervous systems are, however, not generated in this way^3–13. Nishi and Koketsu^3–5 proposed that the slow inhibitory postsynaptic potential (IPSP) in bullfrog sympathetic ganglia is due to a unique mechanism, the synaptic activation of the electrogenic Na pump (see also refs 11–15). In many, if not all, neurones, the outward pumping of sodium is coupled to the inward transport of K, with more Na extruded than K taken in, thus producing an outward movement of positive charge¹⁶. This electrogenic pumping of Na, which is blocked by ouabain or K-free Ringer, produces a hyperpolarisation of the membrane without a change in membrane permeability¹⁶. In the present experiments, the direct role of the electrogenic Na pump in slow synaptic inhibition was tested. The experiments were carried out on the ninth or tenth paravertebral sympathetic ganglion of the bullfrog using the sucrose gap technique. We found that although electrogenic Na pumping was inhibited by ouabain or K-free Ringer, the slow IPSP was not blocked by ouabain and was enhanced by K-free Ringer. The data are consistent with the hypothesis that the slow IPSP may result from an inactivation of Na conductance rather than from an activation of the electrogenic Na pump.