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

Area of Science:

• Neuroscience
• Molecular Biology
• Ion Channel Physiology

Background:

• Serotonin is known to increase potassium conductance in Aplysia neuron R15.
• This effect is mediated by cAMP-dependent protein phosphorylation.
• Neuron R15 possesses multiple distinct potassium channels.

Purpose of the Study:

• To identify the specific potassium channel modulated by serotonin in Aplysia neuron R15.
• To characterize the properties of this serotonin-modulated potassium channel.
• To differentiate this channel from other potassium conductances in the neuron.

Main Methods:

• Voltage clamp analysis of membrane currents.
• Investigation of current reversal potentials and potassium concentration dependence.
• Assessment of cation effects (monovalent and divalent) on channel activity.
• Analysis of voltage dependence of inactivation for other potassium currents.

Main Results:

• The serotonin-modulated potassium channel is an anomalous or inward rectifier (IR).
• This IR channel is partially active at rest and further activated by serotonin.
• Both resting and serotonin-evoked currents exhibit characteristics of anomalous rectification and similar cation dependencies.
• A fast transient potassium current does not account for the anomalous rectification.

Conclusions:

• The inward rectifier potassium channel is the primary mediator of serotonin's effect on potassium conductance in R15.
• This IR channel is distinct from other K+ channels in the neuron.
• Serotonin modulates the activity of these specific inward rectifier potassium channels.