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 K+ channel modulated by serotonin is an anomalous or inward rectifier (designated IR) that is present in R15 together with the 3 other distinct K+ channels previously described for this cell. 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 K+ equilibrium potential, exhibit similar dependences in magnitude on external K+ concentration and display marked anomalous rectification. The effects of particluar monovalent and divalent cations are also similar on the resting and serotonin-evoked currents. Rb+, Cs+ and Ba2+ block both currents; Tl+ can substitute for K+ as a charge carrier and channel activator in both. These properties are characteristic of anomalous rectifiers in other systems. 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 R5. The inward rectifier is therefore a separate current mediated by its own channels, the activity of which can be modulated by serotonin.