Analysis of the modulation by serotonin of a voltage-dependent potassium current in sensory neurons of Aplysia.
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Potassium currents in pleural sensory neurons of Aplysia were studied under control conditions and in the presence of serotonin (5-HT). Using pharmacological techniques we isolated a current that we refer to as IK,V. Although it is not known whether IK,V represents a distinct type of membrane channel, we described its properties using a Hodgkin-Huxley type model. The effects of 5-HT on IK,V were complex. 5-HT decreased by 50% the steady-state magnitude (Iss) of IK,V in response to a voltage-clamp pulse from -50 mV to +20 mV. In addition, 5-HT significantly slowed both activation kinetics (the time constant of activation was increased by 29% at +20 mV) and inactivation kinetics (the time constant of inactivation was increased by 518% at +20 mV). Mathematical descriptions of IK,V in control conditions and in the presence of 5-HT were used to estimate the relative contribution of serotonergic modulation of IK,V to the total 5-HT-induced modulation of membrane currents. Effects of 5-HT on IK,V account for more than 87% of the 5-HT-induced reduction in outward current during the first 20 ms of a voltage-clamp pulse to +20 mV. This result implies that 5-HT exerts many of its effects on spike width in sensory neurons via modulation of IK,V. Effects of 5-HT on IK,V are consistent with a model in which the maximal conductance underlying the current is decreased by 50%, and the rate constants between open and closed states of both the activation and inactivation processes are diminished in magnitude across all membrane potentials.
