Serotonin increases an anomalously rectifying K+ current in the Aplysia neuron R15

Abstract

Previous work has shown that serotonin causes an increase in K+ conductance in the identified Aplysia neuron R15. This response is mediated by cAMP-dependent protein phosphorylation. The results presented here show that the K+ channel modulated by serotonin is an anomalous or inward rectifier (designated IR) that is present in R15 together with the three other distinct K+ channels previously described for this cell. Several lines of evidence indicate that this inward rectifier is partially activated in the resting cell and is further activated by serotonin. Voltage clamp analysis of resting and serotonin-evoked membrane currents at various external K+ concentrations shows that both currents have reversal potentials close to the potassium equilibrium potential, exhibit similar dependences in magnitude on external K+ concentration, and display marked anomalous rectification. The effects of particular monovalent and divalent cations are also similar on the resting and serotonin-evoked currents. Rb+, Cs+, and Ba2+ block both currents while Tl+ can substitute for K+ as a charge carrier and channel activator in both. These properties are characteristics of anomalous rectifiers in other systems. Furthermore, measurement of the voltage dependence of inactivation for the fast transient K+ current shows that this current cannot account for the anomalously rectifying K+ conductance in R15. The inward rectifier is therefore a separate current mediated by its own channels, the activity of which can be modulated by serotonin.